Diabetes mellitus,often known simply asdiabetes,is a group of commonendocrine diseasescharacterized by sustainedhigh blood sugar levels.[10][11]Diabetes is due to either thepancreasnot producing enoughinsulin,or the cells of the body becoming unresponsive to the hormone's effects.[12]Classic symptoms include thirst,polyuria,weight loss, andblurred vision.If left untreated, the disease can lead to various health complications, including disorders of thecardiovascular system,eye,kidney,andnerves.[3]Diabetes accounts for approximately 4.2 million deaths every year,[9]with an estimated 1.5 million caused by either untreated or poorly treated diabetes.[10]

Diabetes mellitus
A hollow circle with a thick blue border and a clear centre
Universal blue circle symbol for diabetes[1]
Pronunciation
SpecialtyEndocrinology
Symptoms
Complications
  • Metabolic imbalances
  • Cardiovascular diseases
  • Nerve and brain damage
  • Kidney failure
  • Gastrointestinal changes[2][3][4][5]
DurationRemission may occur, but diabetes is often life-long
Types
  • Type 1 diabetes
  • Type 2 diabetes
  • Gestational diabetes
CausesInsulin insufficiency or gradual resistance
Risk factors
Diagnostic method
Differential diagnosisdiabetes insipidus
Treatment
Medication
Frequency463 million (5.7%)[9]
Deaths4.2 million (2019)[9]

The major types of diabetes aretype 1andtype 2.[13]The most common treatment for type 1 isinsulin replacement therapy(insulin injections), whileanti-diabetic medications(such asmetforminandsemaglutide) andlifestyle modificationscan be used to manage type 2.Gestational diabetes,a form that arises duringpregnancyin some women, normally resolves shortly after delivery.

As of 2021, an estimated 537 million people had diabetes worldwide accounting for 10.5% of the adult population, with type 2 making up about 90% of all cases. TheWorld Health Organizationhas reported that diabetes was "among the top 10 causes of death in 2021, following a significant percentage increase of 95% since 2000."[14]It is estimated that by 2045, approximately 783 million adults, or 1 in 8, will be living with diabetes, representing a 46% increase from the current figures.[15]The prevalence of the disease continues to increase, most dramatically in low- and middle-income nations.[16]Rates are similar in women and men, with diabetes being the seventh leading cause of death globally.[17][18]The global expenditure on diabetes-related healthcare is an estimated US$760 billion a year.[19]

Signs and symptoms

edit
Overview of the most significant symptoms of diabetes
Retinopathy, nephropathy, and neuropathy are potential complications of diabetes

The classic symptoms of untreated diabetes arepolyuria,thirst, and weight loss.[20]Several other non-specific signs and symptoms may also occur, including fatigue, blurred vision, and genital itchiness due toCandidainfection.[20]About half of affected individuals may also be asymptomatic.[20]Type 1 presents abruptly following a pre-clinical phase, while type 2 has a more insidious onset; patients may remain asymptomatic for many years.[21]

Diabetic ketoacidosisis a medical emergency that occurs most commonly in type 1, but may also occur in type 2 if it has been longstanding or if the individual has significant β-cell dysfunction.[22]Excessive production ofketone bodiesleads to signs and symptoms including nausea, vomiting, abdominal pain, the smell ofacetonein the breath, deep breathing known asKussmaul breathing,and in severe casesdecreased level of consciousness.[22]Hyperosmolar hyperglycemic stateis another emergency characterized by dehydration secondary to severe hyperglycemia, with resultanthypernatremialeading to an altered mental state and possiblycoma.[23]

Hypoglycemiais a recognized complication of insulin treatment used in diabetes.[24]An acute presentation can include mild symptoms such assweating,trembling, andpalpitations,to more serious effects includingimpaired cognition,confusion,seizures,coma,and rarely death.[24]Recurrent hypoglycemic episodes may lower the glycemic threshold at which symptoms occur, meaning mild symptoms may not appear before cognitive deterioration begins to occur.[24]

Long-term complications

edit

The major long-term complications of diabetes relate to damage toblood vesselsat bothmacrovascularandmicrovascularlevels.[25][26]Diabetes doubles the risk ofcardiovascular disease,and about 75% of deaths in people with diabetes are due tocoronary artery disease.[27]Other macrovascular morbidities includestrokeandperipheral artery disease.[28]

Microvascular disease affects theeyes,kidneys,andnerves.[25]Damage to the retina, known asdiabetic retinopathy,is the most common cause of blindness in people of working age.[20]The eyes can also be affected in other ways, including development ofcataractandglaucoma.[20]It is recommended that people with diabetes visit anoptometristorophthalmologistonce a year.[29]

Diabetic nephropathyis a major cause ofchronic kidney disease,accounting for over 50% of patients ondialysisin the United States.[30]Diabetic neuropathy,damage to nerves, manifests in various ways, includingsensory loss,neuropathic pain,andautonomic dysfunction(such aspostural hypotension,diarrhoea,anderectile dysfunction).[20]Loss of pain sensation predisposes to trauma that can lead todiabetic foot problems(such asulceration), the most common cause of non-traumatic lower-limbamputation.[20]

Hearing lossis another long-term complication associated with diabetes.[31]

Based on extensive data and numerous cases of gallstone disease, it appears that a causal link might exist between type 2 diabetes and gallstones. People with diabetes are at a higher risk of developing gallstones compared to those without diabetes.[32]

There is a link betweencognitive deficitand diabetes; studies have shown that diabetic individuals are at a greater risk of cognitive decline, and have a greater rate of decline compared to those without the disease.[33]The condition also predisposes tofalls in the elderly,especially those treated withinsulin.[34]

Causes

edit
Comparison of type 1 and 2 diabetes[35]
Feature Type 1 diabetes Type 2 diabetes
Onset Sudden Gradual
Age at onset Any age; average age at diagnosis being 24.[36] Mostly in adults
Body size Thin or normal[37] Oftenobese
Ketoacidosis Common Rare
Autoantibodies Usually present Absent
Endogenous insulin Low or absent Normal, decreased
or increased
Heritability 0.69 to 0.88[38][39][40] 0.47 to 0.77[41]
Prevalence

(age standardized)

<2 per 1,000[42] ~6% (men), ~5% (women)[43]

Diabetes is classified by theWorld Health Organizationinto six categories:type 1 diabetes,type 2 diabetes,hybrid forms of diabetes (includingslowly evolving, immune-mediated diabetes of adultsandketosis-prone type 2 diabetes), hyperglycemia first detected during pregnancy, "other specific types", and "unclassified diabetes".[44]Diabetes is a more variable disease than once thought, and individuals may have a combination of forms.[45]

Type 1

edit

Type 1 accounts for 5 to 10% of diabetes cases and is the most common type diagnosed in patients under 20 years;[46]however, the older term "juvenile-onset diabetes" is no longer used as onset in adulthood is not unusual.[30]The disease is characterized by loss of the insulin-producingbeta cellsof thepancreatic islets,leading to severe insulin deficiency, and can be further classified asimmune-mediatedoridiopathic(without known cause).[46]The majority of cases are immune-mediated, in which aT cell-mediatedautoimmuneattack causes loss of beta cells and thus insulin deficiency.[47]Patients often have irregular and unpredictable blood sugar levels due to very low insulin and an impaired counter-response to hypoglycemia.[48]

Autoimmune attack in type 1 diabetes.

Type 1 diabetes is partlyinherited,with multiple genes, including certainHLA genotypes,known to influence the risk of diabetes. In genetically susceptible people, the onset of diabetes can be triggered by one or moreenvironmental factors,[49]such as aviral infectionor diet. Several viruses have been implicated, but to date there is no stringent evidence to support this hypothesis in humans.[49][50]

Type 1 diabetes can occur at any age, and a significant proportion is diagnosed during adulthood.Latent autoimmune diabetes of adults(LADA) is the diagnostic term applied when type 1 diabetes develops in adults; it has a slower onset than the same condition in children. Given this difference, some use the unofficial term "type 1.5 diabetes" for this condition. Adults with LADA are frequently initially misdiagnosed as having type 2 diabetes, based on age rather than a cause.[51]LADA leaves adults with higher levels of insulin production than type 1 diabetes, but not enough insulin production for healthy blood sugar levels.[52][53]

Type 2

edit
Reduced insulin secretion or weaker effect of insulin on its receptor leads to high glucose content in the blood.

Type 2 diabetes is characterized byinsulin resistance,which may be combined with relatively reduced insulin secretion.[12]The defective responsiveness of body tissues to insulin is believed to involve theinsulin receptor.[54]However, the specific defects are not known. Diabetes mellitus cases due to a known defect are classified separately. Type 2 diabetes is the most common type of diabetes mellitus accounting for 95% of diabetes.[2]Many people with type 2 diabetes have evidence ofprediabetes(impaired fasting glucose and/or impaired glucose tolerance) before meeting the criteria for type 2 diabetes.[55]The progression of prediabetes to overt type 2 diabetes can be slowed or reversed by lifestyle changes ormedicationsthat improve insulin sensitivity or reduce theliver's glucose production.[56]

Type 2 diabetes is primarily due to lifestyle factors and genetics.[57]A number of lifestyle factors are known to be important to the development of type 2 diabetes, includingobesity(defined by abody mass indexof greater than 30), lack ofphysical activity,poordiet,stress,andurbanization.[35][58]Excess body fat is associated with 30% of cases in people of Chinese and Japanese descent, 60–80% of cases in those of European and African descent, and 100% of Pima Indians and Pacific Islanders.[12]Even those who are not obese may have a highwaist–hip ratio.[12]

Dietary factors such assugar-sweetened drinks are associated with an increased risk.[59][60]The type offatsin the diet is also important, withsaturated fatandtrans fatsincreasing the risk andpolyunsaturatedandmonounsaturated fatdecreasing the risk.[57]Eatingwhite riceexcessively may increase the risk of diabetes, especially in Chinese and Japanese people.[61]Lack of physical activity may increase the risk of diabetes in some people.[62]

Adverse childhood experiences,including abuse, neglect, and household difficulties, increase the likelihood of type 2 diabetes later in life by 32%, withneglecthaving the strongest effect.[63]

Antipsychotic medicationside effects (specifically metabolic abnormalities,dyslipidemiaand weight gain) are also potential risk factors.[64]

Gestational diabetes

edit

Gestational diabetes resembles type 2 diabetes in several respects, involving a combination of relatively inadequate insulin secretion and responsiveness. It occurs in about 2–10% of allpregnanciesand may improve or disappear after delivery.[65]It is recommended that all pregnant women get tested starting around 24–28 weeks gestation.[66]It is most often diagnosed in the second or third trimester because of the increase in insulin-antagonist hormone levels that occurs at this time.[66]However, after pregnancy approximately 5–10% of women with gestational diabetes are found to have another form of diabetes, most commonly type 2.[65]Gestational diabetes is fully treatable, but requires careful medical supervision throughout the pregnancy. Management may include dietary changes, blood glucose monitoring, and in some cases, insulin may be required.[67]

Though it may be transient, untreated gestational diabetes can damage the health of the fetus or mother. Risks to the baby includemacrosomia(high birth weight),congenital heartandcentral nervous systemabnormalities, andskeletal musclemalformations. Increased levels of insulin in a fetus's blood may inhibit fetalsurfactantproduction and causeinfant respiratory distress syndrome.Ahigh blood bilirubin levelmay result fromred blood cell destruction.In severe cases, perinatal death may occur, most commonly as a result of poor placental perfusion due to vascular impairment.Labor inductionmay be indicated with decreased placental function. Acaesarean sectionmay be performed if there is markedfetal distress[68]or an increased risk of injury associated with macrosomia, such asshoulder dystocia.[69]

Other types

edit

Maturity onset diabetes of the young(MODY) is a rareautosomal dominantinherited form of diabetes, due to one of several single-gene mutations causing defects in insulin production.[70]It is significantly less common than the three main types, constituting 1–2% of all cases. The name of this disease refers to early hypotheses as to its nature. Being due to a defective gene, this disease varies in age at presentation and in severity according to the specific gene defect; thus, there are at least 13 subtypes of MODY. People with MODY often can control it without using insulin.[71]

Some cases of diabetes are caused by the body's tissue receptors not responding to insulin (even when insulin levels are normal, which is what separates it from type 2 diabetes); this form is very uncommon. Genetic mutations (autosomalormitochondrial) can lead to defects in beta cell function. Abnormal insulin action may also have been genetically determined in some cases. Any disease that causes extensive damage to the pancreas may lead to diabetes (for example,chronic pancreatitisandcystic fibrosis). Diseases associated with excessive secretion ofinsulin-antagonistichormones can cause diabetes (which is typically resolved once thehormoneexcess is removed). Many drugs impair insulin secretion and some toxins damage pancreatic beta cells, whereas others increaseinsulin resistance(especiallyglucocorticoidswhich can provoke "steroid diabetes"). TheICD-10(1992) diagnostic entity,malnutrition-related diabetes mellitus(ICD-10 code E12), was deprecated by theWorld Health Organization(WHO) when the current taxonomy was introduced in 1999.[72]Yet another form of diabetes that people may develop isdouble diabetes.This is when a type 1 diabetic becomes insulin resistant, the hallmark for type 2 diabetes or has a family history for type 2 diabetes.[73]It was first discovered in 1990 or 1991.

The following is a list of disorders that may increase the risk of diabetes:[74]

Pathophysiology

edit
The fluctuation ofblood sugar(red) and the sugar-lowering hormoneinsulin(blue) in humans during the course of a day with three meals. One of the effects of asugar-rich vs astarch-rich meal is highlighted.
Mechanism of insulin release in normal pancreaticbeta cells.Insulin production is more or less constant within the beta cells. Its release is triggered by food, chiefly food containing absorbable glucose.

Insulinis the principal hormone that regulates the uptake ofglucosefrom the blood into most cells of the body, especially liver, adipose tissue and muscle, except smooth muscle, in which insulin acts via theIGF-1.[76]Therefore, deficiency of insulin or the insensitivity of itsreceptorsplay a central role in all forms of diabetes mellitus.[77]

The body obtains glucose from three main sources: the intestinal absorption of food; the breakdown ofglycogen(glycogenolysis), the storage form of glucose found in the liver; andgluconeogenesis,the generation of glucose from non-carbohydrate substrates in the body.[78]Insulin plays a critical role in regulating glucose levels in the body. Insulin can inhibit the breakdown of glycogen or the process of gluconeogenesis, it can stimulate the transport of glucose into fat and muscle cells, and it can stimulate the storage of glucose in the form of glycogen.[78]

Insulin is released into the blood by beta cells (β-cells), found in theislets of Langerhansin the pancreas, in response to rising levels of blood glucose, typically after eating. Insulin is used by about two-thirds of the body's cells to absorb glucose from the blood for use as fuel, for conversion to other needed molecules, or for storage. Lower glucose levels result in decreased insulin release from the beta cells and in the breakdown of glycogen to glucose. This process is mainly controlled by the hormoneglucagon,which acts in the opposite manner to insulin.[79]

If the amount of insulin available is insufficient, or if cells respond poorly to the effects of insulin (insulin resistance), or if the insulin itself is defective, then glucose is not absorbed properly by the body cells that require it, and is not stored appropriately in the liver and muscles. The net effect is persistently high levels of blood glucose, poorprotein synthesis,and other metabolic derangements, such as metabolicacidosisin cases of complete insulin deficiency.[78]

When there is too much glucose in the blood for a long time, thekidneyscannot absorb it all (reach a threshold ofreabsorption) and the extra glucose gets passed out of the body throughurine(glycosuria).[80]This increases theosmotic pressureof the urine and inhibits reabsorption of water by the kidney, resulting in increased urine production (polyuria) and increased fluid loss. Lost blood volume is replaced osmotically from water in body cells and other body compartments, causingdehydrationand increased thirst (polydipsia).[78]In addition, intracellular glucose deficiency stimulates appetite leading to excessive food intake (polyphagia).[81]

Diagnosis

edit

Diabetes mellitus is diagnosed with a test for the glucose content in the blood, and is diagnosed by demonstrating any one of the following:[72]

  • Fasting plasma glucose level≥ 7.0 mmol/L (126 mg/dL). For this test, blood is taken after a period of fasting, i.e. in the morning before breakfast, after the patient had sufficient time to fast overnight or at least 8 hours before the test.
  • Plasma glucose≥ 11.1 mmol/L (200 mg/dL) two hours after a 75 gram oral glucose load as in aglucose tolerance test(OGTT)
  • Symptoms of high blood sugar and plasma glucose ≥ 11.1 mmol/L (200 mg/dL) either while fasting or not fasting
  • Glycated hemoglobin(HbA1C) ≥ 48 mmol/mol (≥ 6.5DCCT%).[82]
WHO diabetes diagnostic criteria[83][84] edit
Condition 2-hour glucose Fasting glucose HbA1c
Unit mmol/L mg/dL mmol/L mg/dL mmol/mol DCCT %
Normal < 7.8 < 140 < 6.1 < 110 < 42 < 6.0
Impaired fasting glycaemia < 7.8 < 140 6.1–7.0 110–125 42–46 6.0–6.4
Impaired glucose tolerance ≥ 7.8 ≥ 140 < 7.0 < 126 42–46 6.0–6.4
Diabetes mellitus ≥ 11.1 ≥ 200 ≥ 7.0 ≥ 126 ≥ 48 ≥ 6.5

A positive result, in the absence of unequivocal high blood sugar, should be confirmed by a repeat of any of the above methods on a different day. It is preferable to measure a fasting glucose level because of the ease of measurement and the considerable time commitment of formal glucose tolerance testing, which takes two hours to complete and offers no prognostic advantage over the fasting test.[85]According to the current definition, two fasting glucose measurements at or above 7.0 mmol/L (126 mg/dL) is considered diagnostic for diabetes mellitus.

Per the WHO, people with fasting glucose levels from 6.1 to 6.9 mmol/L (110 to 125 mg/dL) are considered to haveimpaired fasting glucose.[86]People with plasma glucose at or above 7.8 mmol/L (140 mg/dL), but not over 11.1 mmol/L (200 mg/dL), two hours after a 75 gram oral glucose load are considered to haveimpaired glucose tolerance.Of these two prediabetic states, the latter in particular is a major risk factor for progression to full-blown diabetes mellitus, as well as cardiovascular disease.[87]TheAmerican Diabetes Association(ADA) since 2003 uses a slightly different range for impaired fasting glucose of 5.6 to 6.9 mmol/L (100 to 125 mg/dL).[88]

Glycated hemoglobinis better thanfasting glucosefor determining risks of cardiovascular disease and death from any cause.[89]

Prevention

edit

There is no knownpreventivemeasure for type 1 diabetes.[2]However, islet autoimmunity and multiple antibodies can be a strong predictor of the onset of type 1 diabetes.[90]Type 2 diabetes—which accounts for 85–90% of all cases worldwide—can often be prevented or delayed[91]by maintaining anormal body weight,engaging in physical activity, and eating a healthy diet.[2]Higher levels of physical activity (more than 90 minutes per day) reduce the risk of diabetes by 28%.[92]Dietary changes known to be effective in helping to prevent diabetes include maintaining a diet rich inwhole grainsandfiber,and choosing good fats, such as thepolyunsaturated fatsfound in nuts, vegetable oils, and fish.[93]Limiting sugary beverages and eating less red meat and other sources ofsaturated fatcan also help prevent diabetes.[93]Tobacco smoking is also associated with an increased risk of diabetes and its complications, sosmoking cessationcan be an important preventive measure as well.[94]

The relationship between type 2 diabetes and the main modifiable risk factors (excess weight, unhealthy diet, physical inactivity and tobacco use) is similar in all regions of the world. There is growing evidence that the underlying determinants of diabetes are a reflection of the major forces driving social, economic and cultural change:globalization,urbanization, population aging, and the generalhealth policyenvironment.[95]

Comorbidity

edit

Diabetes patients' comorbidities have a significant impact on medical expenses and related costs. It has been demonstrated that patients with diabetes are more likely to experience respiratory, urinary tract, and skin infections, develop atherosclerosis, hypertension, and chronic kidney disease, putting them at increased risk of infection and complications that require medical attention.[96]Patients with diabetes mellitus are more likely to experience certain infections, such as COVID-19, with prevalence rates ranging from 5.3 to 35.5%.[97][98]Maintaining adequate glycemic control is the primary goal of diabetes management since it is critical to managing diabetes and preventing or postponing such complications.[99]

Management

edit

Diabetes management concentrates on keeping blood sugar levels close to normal, without causing low blood sugar.[100]This can usually be accomplished with dietary changes,[101]exercise, weight loss, and use of appropriate medications (insulin, oral medications).[100]

Learning about the disease and actively participating in the treatment is important, since complications are far less common and less severe in people who have well-managed blood sugar levels.[100][102]The goal of treatment is an A1C level below 7%.[103][104]Attention is also paid to other health problems that may accelerate the negative effects of diabetes. These includesmoking,high blood pressure,metabolic syndromeobesity,and lack of regularexercise.[100][105]Specialized footwearis widely used to reduce the risk ofdiabetic foot ulcersby relieving the pressure on the foot.[106][107][108]Foot examination for patients living with diabetes should be done annually which includes sensation testing, footbiomechanics,vascular integrity and foot structure.[109]

Concerning those with severemental illness,the efficacy oftype 2 diabetesself-management interventions is still poorly explored, with insufficient scientific evidence to show whether these interventions have similar results to those observed in the general population.[110]

Lifestyle

edit

People with diabetes can benefit from education about the disease and treatment, dietary changes, and exercise, with the goal of keeping both short-term and long-term blood glucose levelswithin acceptable bounds.In addition, given the associated higher risks of cardiovascular disease, lifestyle modifications are recommended to control blood pressure.[111][112]

Weight losscan prevent progression from prediabetes todiabetes type 2,decrease the risk of cardiovascular disease, or result in a partial remission in people with diabetes.[113][114]No single dietary pattern is best for all people with diabetes.[115]Healthy dietary patterns, such as theMediterranean diet,low-carbohydrate diet,orDASH diet,are often recommended, although evidence does not support one over the others.[113][114]According to the ADA, "reducing overall carbohydrate intake for individuals with diabetes has demonstrated the most evidence for improving glycemia", and for individuals with type 2 diabetes who cannot meet the glycemic targets or where reducing anti-glycemic medications is a priority,low or very-low carbohydrate dietsare a viable approach.[114]For overweight people with type 2 diabetes, any diet that achieves weight loss is effective.[115][116]

A 2020 Cochrane systematic review compared several non-nutritive sweeteners to sugar, placebo and a nutritive low-calorie sweetener (tagatose), but the results were unclear for effects on HbA1c, body weight and adverse events.[117]The studies included were mainly of very low-certainty and did not report on health-related quality of life, diabetes complications, all-cause mortality or socioeconomic effects.[117]

Medications

edit

Glucose control

edit

Most medications used to treat diabetes act by loweringblood sugar levelsthrough different mechanisms. There is broad consensus that when people with diabetes maintain tight glucose control – keeping the glucose levels in their blood within normal ranges – they experience fewer complications, such askidney problemsoreye problems.[118][119]There is, however, debate as to whether this is appropriate andcost effectivefor people later in life in whom the risk of hypoglycemia may be more significant.[120]

There are a number of different classes of anti-diabetic medications. Type 1 diabetes requires treatment withinsulin,ideally using a "basal bolus" regimen that most closely matches normal insulin release: long-acting insulin for thebasal rateand short-acting insulin with meals.[121]Type 2 diabetes is generally treated with medication that is taken by mouth (e.g.metformin) although some eventually require injectable treatment with insulin orGLP-1 agonists.[122]

Metforminis generally recommended as a first-line treatment for type 2 diabetes, as there is good evidence that it decreases mortality.[7]It works by decreasing the liver's production of glucose, and increasing the amount of glucose stored in peripheral tissue.[123]Several other groups of drugs, mainly oral medication, may also decrease blood sugar in type 2 diabetes. These include agents that increase insulin release (sulfonylureas), agents that decrease absorption of sugar from the intestines (acarbose), agents that inhibit the enzyme dipeptidyl peptidase-4 (DPP-4) that inactivates incretins such as GLP-1 and GIP (sitagliptin), agents that make the body more sensitive to insulin (thiazolidinedione) and agents that increase the excretion of glucose in the urine (SGLT2 inhibitors).[123]When insulin is used in type 2 diabetes, a long-acting formulation is usually added initially, while continuing oral medications.[7]

Some severe cases of type 2 diabetes may also be treated with insulin, which is increased gradually until glucose targets are reached.[7][124]

Blood pressure lowering

edit

Cardiovascular diseaseis a serious complication associated with diabetes, and many international guidelines recommend blood pressure treatment targets that are lower than 140/90 mmHg for people with diabetes.[125]However, there is only limited evidence regarding what the lower targets should be. A 2016 systematic review found potential harm to treating to targets lower than 140 mmHg,[126]and a subsequent systematic review in 2019 found no evidence of additional benefit from blood pressure lowering to between 130 – 140mmHg, although there was an increased risk of adverse events.[127]

2015 American Diabetes Association recommendations are that people with diabetes and albuminuria should receive an inhibitor of the renin-angiotensin system to reduce the risks of progression to end-stage renal disease, cardiovascular events, and death.[128]There is some evidence thatangiotensin converting enzyme inhibitors(ACEIs) are superior to other inhibitors of the renin-angiotensin system such asangiotensin receptor blockers(ARBs),[129]oraliskirenin preventing cardiovascular disease.[130]Although a more recent review found similar effects of ACEIs and ARBs on major cardiovascular and renal outcomes.[131]There is no evidence that combining ACEIs and ARBs provides additional benefits.[131]

Aspirin

edit

The use ofaspirinto prevent cardiovascular disease in diabetes is controversial.[128]Aspirin is recommended by some in people at high risk of cardiovascular disease; however, routine use of aspirin has not been found to improve outcomes in uncomplicated diabetes.[132]2015 American Diabetes Association recommendations for aspirin use (based on expert consensus or clinical experience) are that low-dose aspirin use is reasonable in adults with diabetes who are at intermediate risk of cardiovascular disease (10-year cardiovascular disease risk, 5–10%).[128]National guidelines for England and Wales by theNational Institute for Health and Care Excellence(NICE) recommend against the use of aspirin in people with type 1 or type 2 diabetes who do not have confirmed cardiovascular disease.[121][122]

Surgery

edit

Weight loss surgeryin those withobesityand type 2 diabetes is often an effective measure.[133]Many are able to maintain normal blood sugar levels with little or no medications following surgery[134]and long-term mortality is decreased.[135]There is, however, a short-term mortality risk of less than 1% from the surgery.[136]Thebody mass indexcutoffs for when surgery is appropriate are not yet clear.[135]It is recommended that this option be considered in those who are unable to get both their weight and blood sugar under control.[137]

Apancreas transplantis occasionally considered for people with type 1 diabetes who have severe complications of their disease, includingend stage kidney diseaserequiringkidney transplantation.[138]

Diabetic peripheral neuropathy(DPN) affects 30% of all diabetes patients.[139]When DPN is superimposed withnerve compression,DPN may be treatable with multiplenerve decompressions.[140][141]The theory is that DPN predisposesperipheral nervesto compression at anatomical sites of narrowing, and that the majority of DPN symptoms are actually attributable to nerve compression, a treatable condition, rather than DPN itself.[142][143]The surgery is associated with lowerpain scores,highertwo-point discrimination(a measure of sensory improvement), lower rate ofulcerations,fewer falls (in the case of lower extremity decompression), and feweramputations.[143][144][145][141]

Self-management and support

edit

In countries using ageneral practitionersystem, such as the United Kingdom, care may take place mainly outside hospitals, with hospital-based specialist care used only in case of complications, difficult blood sugar control, or research projects. In other circumstances, general practitioners and specialists share care in a team approach. Evidence has shown that social prescribing led to slight improvements in blood sugar control for people with type 2 diabetes.[146]Hometelehealthsupport can be an effective management technique.[147]

The use oftechnologyto deliver educational programs for adults with type 2 diabetes includes computer-based self-management interventions to collect for tailored responses to facilitate self-management.[148]There is no adequate evidence to support effects oncholesterol,blood pressure,behavioral change(such asphysical activitylevels and dietary),depression,weight andhealth-related quality of life,nor in other biological, cognitive or emotional outcomes.[148][149]

Epidemiology

edit
Rates of diabetes worldwide in 2014. The worldwide prevalence was 9.2%.
Mortality rate of diabetes worldwide in 2012 per million inhabitants
28–91
92–114
115–141
142–163
164–184
185–209
210–247
248–309
310–404
405–1879

In 2017, 425 million people had diabetes worldwide,[150]up from an estimated 382 million people in 2013[151]and from 108 million in 1980.[152]Accounting for the shifting age structure of the global population, the prevalence of diabetes is 8.8% among adults, nearly double the rate of 4.7% in 1980.[150][152]Type 2 makes up about 90% of the cases.[17][35]Some data indicate rates are roughly equal in women and men,[17]but male excess in diabetes has been found in many populations with higher type 2 incidence, possibly due to sex-related differences in insulin sensitivity, consequences of obesity and regional body fat deposition, and other contributing factors such as high blood pressure, tobacco smoking, and alcohol intake.[153][154]

The WHO estimates that diabetes resulted in 1.5 million deaths in 2012, making it the 8th leading cause of death.[155][152]However, another 2.2 million deaths worldwide were attributable to high blood glucose and the increased risks of cardiovascular disease and other associated complications (e.g. kidney failure), which often lead to premature death and are often listed as the underlying cause on death certificates rather than diabetes.[152][156]For example, in 2017, theInternational Diabetes Federation(IDF) estimated that diabetes resulted in 4.0 million deaths worldwide,[150]using modeling to estimate the total number of deaths that could be directly or indirectly attributed to diabetes.[150]

Diabetes occurs throughout the world but is more common (especially type 2) in more developed countries. The greatest increase in rates has, however, been seen in low- and middle-income countries,[152]where more than 80% of diabetic deaths occur.[157]The fastest prevalence increase is expected to occur in Asia and Africa, where most people with diabetes will probably live in 2030.[158]The increase in rates in developing countries follows the trend of urbanization and lifestyle changes, including increasingly sedentary lifestyles, less physically demanding work and the global nutrition transition, marked by increased intake of foods that are high energy-dense but nutrient-poor (often high in sugar and saturated fats, sometimes referred to as the "Western-style" diet).[152][158]The global number of diabetes cases might increase by 48% between 2017 and 2045.[150]

As of 2020, 38% of all US adults had prediabetes.[159]Prediabetesis an early stage of diabetes.

History

edit

Diabetes was one of the first diseases described,[160]with anEgyptianmanuscript fromc.1500BCEmentioning "too great emptying of the urine."[161]TheEbers papyrusincludes a recommendation for a drink to take in such cases.[162]The first described cases are believed to have been type 1 diabetes.[161]Indian physicians around the same time identified the disease and classified it asmadhumehaor "honey urine", noting the urine would attract ants.[161][162]

The term "diabetes" or "to pass through" was first used in 230 BCE by the GreekApollonius of Memphis.[161]The disease was considered rare during the time of theRoman empire,withGalencommenting he had only seen two cases during his career.[161]This is possibly due to the diet and lifestyle of the ancients, or because the clinical symptoms were observed during the advanced stage of the disease. Galen named the disease "diarrhea of the urine" (diarrhea urinosa).[163]

The earliest surviving work with a detailed reference to diabetes is that ofAretaeus of Cappadocia(2nd or early 3rdcentury CE). He described the symptoms and the course of the disease, which he attributed to the moisture and coldness, reflecting the beliefs of the "Pneumatic School".He hypothesized a correlation between diabetes and other diseases, and he discussed differential diagnosis from the snakebite, which also provokes excessive thirst. His work remained unknown in the West until 1552, when the first Latin edition was published in Venice.[163]

Two types of diabetes were identified as separate conditions for the first time by the Indian physiciansSushrutaandCharakain 400–500 CE with one type being associated with youth and another type with being overweight.[161]Effective treatment was not developed until the early part of the 20th century when CanadiansFrederick BantingandCharles Bestisolated and purified insulin in 1921 and 1922.[161]This was followed by the development of the long-acting insulinNPHin the 1940s.[161]

Etymology

edit

The worddiabetes(/ˌd.əˈbtz/or/ˌd.əˈbtɪs/) comes fromLatindiabētēs,which in turn comes fromAncient Greekδιαβήτης(diabētēs), which literally means "a passer through; asiphon".[164]Ancient GreekphysicianAretaeus of Cappadocia(fl.1stcenturyCE) used that word, with the intended meaning "excessive discharge of urine", as the name for the disease.[165][166]Ultimately, the word comes from Greekδιαβαίνειν(diabainein), meaning "to pass through",[164]which is composed ofδια- (dia-), meaning "through" andβαίνειν(bainein), meaning "to go".[165]The word "diabetes" is first recorded in English, in the formdiabete,in a medical text written around 1425.

The wordmellitus(/məˈltəs/or/ˈmɛlɪtəs/) comes from the classical Latin wordmellītus,meaning "mellite"[167](i.e. sweetened with honey;[167]honey-sweet[168]). The Latin word comes frommell-, which comes frommel,meaning "honey";[167][168]sweetness;[168]pleasant thing,[168]and the suffix -ītus,[167]whose meaning is the same as that of the English suffix "-ite".[169]It wasThomas Williswho in 1675 added "mellitus" to the word "diabetes" as a designation for the disease, when he noticed the urine of a person with diabetes had a sweet taste (glycosuria). This sweet taste had been noticed in urine by the ancient Greeks, Chinese, Egyptians, and Indians.[170]

Society and culture

edit

The 1989 "St. Vincent Declaration"[171][172]was the result of international efforts to improve the care accorded to those with diabetes. Doing so is important not only in terms of quality of life and life expectancy but also economically – expenses due to diabetes have been shown to be a major drain on health – and productivity-related resources for healthcare systems and governments.

Several countries established more and less successful national diabetes programmes to improve treatment of the disease.[173]

Diabetes stigma

edit

Diabetes stigma describes the negative attitudes, judgment, discrimination, or prejudice against people with diabetes. Often, the stigma stems from the idea that diabetes (particularly Type 2 diabetes) resulted from poor lifestyle and unhealthy food choices rather than other causal factors like genetics and social determinants of health.[174]Manifestation of stigma can be seen throughout different cultures and contexts. Scenarios include diabetes statuses affecting marriage proposals, workplace-employment, and social standing in communities.[175]

Stigma is also seen internally, as people with diabetes can also have negative beliefs about themselves. Often these cases of self-stigma are associated with higher diabetes-specific distress, lower self-efficacy, and poorer provider-patient interactions during diabetes care.[176]

Racial and economic inequalities

edit

Racial and ethnic minorities are disproportionately affected with higher prevalence of diabetes compared to non-minority individuals.[177]While US adults overall have a 40% chance of developing type 2 diabetes, Hispanic/Latino adults chance is more than 50%.[178]African Americans also are much more likely to be diagnosed with diabetes compared to White Americans. Asians have increased risk of diabetes as diabetes can develop at lower BMI due to differences in visceral fat compared to other races. For Asians, diabetes can develop at a younger age and lower body fat compared to other groups. Additionally, diabetes is highly underreported in Asian American people, as 1 in 3 cases are undiagnosed compared to the average 1 in 5 for the nation.[179]

People with diabetes who have neuropathic symptoms such as numbness or tingling in feet or hands are twice as likely to beunemployedas those without the symptoms.[180]

In 2010, diabetes-related emergency room (ER) visit rates in the United States were higher among people from the lowest income communities (526 per 10,000 population) than from the highest income communities (236 per 10,000 population). Approximately 9.4% of diabetes-related ER visits were for the uninsured.[181]

Naming

edit

The term "type 1 diabetes" has replaced several former terms, including childhood-onset diabetes, juvenile diabetes, and insulin-dependent diabetes mellitus. Likewise, the term "type 2 diabetes" has replaced several former terms, including adult-onset diabetes, obesity-related diabetes, and noninsulin-dependent diabetes mellitus. Beyond these two types, there is no agreed-upon standard nomenclature.[182]

Diabetes mellitus is also occasionally known as "sugar diabetes" to differentiate it fromdiabetes insipidus.[183]

Other animals

edit

Diabetes can occur in mammals or reptiles.[184][185]Birds do not develop diabetes because of their unusually high tolerance for elevated blood glucose levels.[186]

In animals, diabetes is most commonly encountered in dogs and cats. Middle-aged animals are most commonly affected. Female dogs are twice as likely to be affected as males, while according to some sources, male cats are more prone than females. In both species, all breeds may be affected, but some small dog breeds are particularly likely to develop diabetes, such asMiniature Poodles.[187]

Feline diabetes is strikingly similar to human type 2 diabetes. TheBurmese,Russian Blue,Abyssinian,andNorwegian Forestcat breeds are at higher risk than other breeds. Overweight cats are also at higher risk.[188]

The symptoms may relate to fluid loss and polyuria, but the course may also be insidious. Diabetic animals are more prone to infections. The long-term complications recognized in humans are much rarer in animals. The principles of treatment (weight loss, oral antidiabetics, subcutaneous insulin) and management of emergencies (e.g. ketoacidosis) are similar to those in humans.[187]

See also

edit

References

edit
  1. ^"Diabetes Blue Circle Symbol".International Diabetes Federation. 17 March 2006. Archived fromthe originalon 5 August 2007.
  2. ^abcdefgh"Diabetes".who.int.Archivedfrom the original on 26 February 2023.Retrieved1 October2022.
  3. ^abKitabchi AE, Umpierrez GE, Miles JM, Fisher JN (July 2009)."Hyperglycemic crises in adult patients with diabetes".Diabetes Care.32(7): 1335–1343.doi:10.2337/dc09-9032.PMC2699725.PMID19564476.Archivedfrom the original on 2016-06-25.
  4. ^Krishnasamy S, Abell TL (July 2018)."Diabetic Gastroparesis: Principles and Current Trends in Management".Diabetes Therapy.9(Suppl 1): 1–42.doi:10.1007/s13300-018-0454-9.ISSN1869-6961.PMC6028327.PMID29934758.
  5. ^Saedi E, Gheini MR, Faiz F, Arami MA (September 2016)."Diabetes mellitus and cognitive impairments".World Journal of Diabetes.7(17): 412–422.doi:10.4239/wjd.v7.i17.412.PMC5027005.PMID27660698.
  6. ^ab"Causes of Diabetes – NIDDK".National Institute of Diabetes and Digestive and Kidney Diseases.June 2014.Archivedfrom the original on 2 February 2016.Retrieved10 February2016.
  7. ^abcdRipsin CM, Kang H, Urban RJ (January 2009)."Management of blood glucose in type 2 diabetes mellitus"(PDF).American Family Physician.79(1): 29–36.PMID19145963.Archived(PDF)from the original on 2013-05-05.
  8. ^Brutsaert EF (February 2017)."Drug Treatment of Diabetes Mellitus".MSDManuals.Archivedfrom the original on 12 October 2018.Retrieved12 October2018.
  9. ^abc"IDF DIABETES ATLAS Ninth Edition 2019"(PDF).diabetesatlas.org.Archived(PDF)from the original on 1 May 2020.Retrieved18 May2020.
  10. ^ab"Diabetes".World Health Organization.Archivedfrom the original on 29 January 2023.Retrieved29 January2023.
  11. ^"Diabetes Mellitus (DM) – Hormonal and Metabolic Disorders".MSD Manual Consumer Version.Archivedfrom the original on 1 October 2022.Retrieved1 October2022.
  12. ^abcdShoback DG, Gardner D, eds. (2011). "Chapter 17".Greenspan's basic & clinical endocrinology(9th ed.). New York: McGraw-Hill Medical.ISBN978-0-07-162243-1.
  13. ^"Symptoms and Causes of Diabetes".National Institute of Diabetes and Digestive and Kidney Diseases, US National Institutes of Health. 2024.Retrieved16 May2024.
  14. ^"The top 10 causes of death".who.int.Retrieved2024-08-12.
  15. ^"Facts & figures".International Diabetes Federation.Archivedfrom the original on 2023-08-10.Retrieved2023-08-10.
  16. ^De Silva AP, De Silva SH, Haniffa R, Liyanage IK, Jayasinghe S, Katulanda P, et al. (April 2018)."Inequalities in the prevalence of diabetes mellitus and its risk factors in Sri Lanka: a lower middle income country".International Journal for Equity in Health.17(1): 45.doi:10.1186/s12939-018-0759-3.PMC5905173.PMID29665834.
  17. ^abcVos T, Flaxman AD, Naghavi M, Lozano R, Michaud C, Ezzati M, et al. (December 2012)."Years lived with disability (YLDs) for 1160 sequelae of 289 diseases and injuries 1990–2010: a systematic analysis for the Global Burden of Disease Study 2010".Lancet.380(9859): 2163–2196.doi:10.1016/S0140-6736(12)61729-2.PMC6350784.PMID23245607.
  18. ^"The top 10 causes of death".who.int.Archivedfrom the original on 24 September 2021.Retrieved18 May2020.
  19. ^Bommer C, Sagalova V, Heesemann E, Manne-Goehler J, Atun R, Bärnighausen T, et al. (May 2018)."Global Economic Burden of Diabetes in Adults: Projections From 2015 to 2030".Diabetes Care.41(5): 963–970.doi:10.2337/dc17-1962.PMID29475843.S2CID3538441.
  20. ^abcdefgFeather, Adam; Randall, David; Waterhouse, Mona (2021).Kumar and Clark's Clinical Medicine(10th ed.).Elsevier.pp. 699–741.ISBN978-0-7020-7868-2.
  21. ^Goldman, Lee; Schafer, Andrew (2020).Goldman-Cecil Medicine(26th ed.).Elsevier.pp. 1490–1510.ISBN978-0-323-53266-2.
  22. ^abPenman, Ian; Ralston, Stuart; Strachan, Mark; Hobson, Richard (2023).Davidson's Principles and Practice of Medicine(24th ed.). Elsevier. pp. 703–753.ISBN978-0-7020-8348-8.
  23. ^Willix, Clare; Griffiths, Emma; Singleton, Sally (May 2019)."Hyperglycaemic presentations in type 2 diabetes".Australian Journal of General Practice.48(5): 263–267.doi:10.31128/AJGP-12-18-4785.PMID31129935.S2CID167207067.Archivedfrom the original on 2023-08-10.Retrieved2023-08-10.
  24. ^abcAmiel, Stephanie A. (2021-05-01)."The consequences of hypoglycaemia".Diabetologia.64(5): 963–970.doi:10.1007/s00125-020-05366-3.ISSN1432-0428.PMC8012317.PMID33550443.
  25. ^ab"Diabetes – long-term effects".Better Health Channel.Victoria: Department of Health.Archivedfrom the original on 2023-10-29.Retrieved2023-08-12.
  26. ^Sarwar N, Gao P, Seshasai SR, Gobin R, Kaptoge S, Di Angelantonio E, et al. (June 2010)."Diabetes mellitus, fasting blood glucose concentration, and risk of vascular disease: a collaborative meta-analysis of 102 prospective studies".Lancet.375(9733): 2215–2222.doi:10.1016/S0140-6736(10)60484-9.PMC2904878.PMID20609967.
  27. ^O'Gara PT, Kushner FG, Ascheim DD, Casey DE, Chung MK, de Lemos JA, et al. (January 2013)."2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines".Circulation.127(4): e368.doi:10.1161/CIR.0b013e3182742cf6.PMID23247304.
  28. ^Papatheodorou K, Banach M, Bekiari E, Rizzo M, Edmonds M (11 March 2018)."Complications of Diabetes 2017".Journal of Diabetes Research.2018:3086167.doi:10.1155/2018/3086167.PMC5866895.PMID29713648.
  29. ^"Diabetes eye care".MedlinePlus.Maryland: National Library of Medicine.Archivedfrom the original on 2018-03-28.Retrieved2018-03-27.
  30. ^abWing, Edward J; Schiffman, Fred (2022).Cecil Essentials of Medicine(10th ed.). Pennsylvania:Elsevier.pp. 282–297, 662–677.ISBN978-0-323-72271-1.
  31. ^Mittal, Rahul; McKenna, Keelin; Keith, Grant; Lemos, Joana R. N.; Mittal, Jeenu; Hirani, Khemraj (9 February 2024)."A systematic review of the association of Type I diabetes with sensorineural hearing loss".PLOS One.19(2): e0298457.Bibcode:2024PLoSO..1998457M.doi:10.1371/journal.pone.0298457.PMC10857576.PMID38335215.
  32. ^Yuan, Shuai; Gill, Dipender; Giovannucci, Edward L.; Larsson, Susanna C. (March 2022)."Obesity, Type 2 Diabetes, Lifestyle Factors, and Risk of Gallstone Disease: A Mendelian Randomization Investigation".Clinical Gastroenterology and Hepatology.20(3): e529–e537.doi:10.1016/j.cgh.2020.12.034.hdl:10044/1/86461.PMID33418132.
  33. ^Cukierman T, Gerstein HC, Williamson JD (December 2005)."Cognitive decline and dementia in diabetes—systematic overview of prospective observational studies".Diabetologia.48(12): 2460–2469.doi:10.1007/s00125-005-0023-4.PMID16283246.
  34. ^Yang Y, Hu X, Zhang Q, Zou R (November 2016)."Diabetes mellitus and risk of falls in older adults: a systematic review and meta-analysis".Age and Ageing.45(6): 761–767.doi:10.1093/ageing/afw140.PMID27515679.
  35. ^abcWilliams textbook of endocrinology(12th ed.). Elsevier/Saunders. 2011. pp. 1371–1435.ISBN978-1-4377-0324-5.
  36. ^"Over a Third of Adults With Type 1 Diabetes Weren't Diagnosed Until After 30".U.S. News & World Report.28 September 2023.Retrieved3 June2024.
  37. ^Lambert P, Bingley PJ (2002). "What is Type 1 Diabetes?".Medicine.30:1–5.doi:10.1383/medc.30.1.1.28264.
  38. ^Skov J, Eriksson D, Kuja-Halkola R, Höijer J, Gudbjörnsdottir S, Svensson AM, et al. (May 2020)."Co-aggregation and heritability of organ-specific autoimmunity: a population-based twin study".European Journal of Endocrinology.182(5): 473–480.doi:10.1530/EJE-20-0049.PMC7182094.PMID32229696.
  39. ^Hyttinen V, Kaprio J, Kinnunen L, Koskenvuo M, Tuomilehto J (April 2003)."Genetic liability of type 1 diabetes and the onset age among 22,650 young Finnish twin pairs: a nationwide follow-up study".Diabetes.52(4): 1052–1055.doi:10.2337/diabetes.52.4.1052.PMID12663480.
  40. ^Condon J, Shaw JE, Luciano M, Kyvik KO, Martin NG, Duffy DL (February 2008)."A study of diabetes mellitus within a large sample of Australian twins"(PDF).Twin Research and Human Genetics.11(1): 28–40.doi:10.1375/twin.11.1.28.PMID18251672.S2CID18072879.Archived(PDF)from the original on 2023-07-01.Retrieved2021-12-27.
  41. ^Willemsen G, Ward KJ, Bell CG, Christensen K, Bowden J, Dalgård C, et al. (December 2015)."The Concordance and Heritability of Type 2 Diabetes in 34,166 Twin Pairs From International Twin Registers: The Discordant Twin (DISCOTWIN) Consortium".Twin Research and Human Genetics.18(6): 762–771.doi:10.1017/thg.2015.83.PMID26678054.S2CID17854531.
  42. ^Lin X, Xu Y, Pan X, Xu J, Ding Y, Sun X, et al. (September 2020)."Global, regional, and national burden and trend of diabetes in 195 countries and territories: an analysis from 1990 to 2025".Scientific Reports.10(1): 14790.Bibcode:2020NatSR..1014790L.doi:10.1038/s41598-020-71908-9.PMC7478957.PMID32901098.
  43. ^Tinajero MG, Malik VS (September 2021). "An Update on the Epidemiology of Type 2 Diabetes: A Global Perspective".Endocrinology and Metabolism Clinics of North America.50(3): 337–355.doi:10.1016/j.ecl.2021.05.013.PMID34399949.
  44. ^Classification of diabetes mellitus 2019(Report). Geneva: World Health Organisation. 2019.ISBN978-92-4-151570-2.Archivedfrom the original on 2023-03-06.Retrieved2023-08-15.
  45. ^Tuomi T, Santoro N, Caprio S, Cai M, Weng J, Groop L (March 2014). "The many faces of diabetes: a disease with increasing heterogeneity".Lancet.383(9922): 1084–1094.doi:10.1016/S0140-6736(13)62219-9.PMID24315621.S2CID12679248.
  46. ^abKumar, V; Abbas, A; Aster, J (2021).Robbins & Cotran Pathologic Basis of Disease(10th ed.). Pennsylvania:Elsevier.pp. 1065–1132.ISBN978-0-323-60992-0.
  47. ^Rother KI (April 2007)."Diabetes treatment—bridging the divide".The New England Journal of Medicine.356(15): 1499–1501.doi:10.1056/NEJMp078030.PMC4152979.PMID17429082.
  48. ^Brutsaert, EF (September 2022)."Diabetes Mellitus (DM)".MSD Manual Professional Version.Merck Publishing.Archivedfrom the original on 2023-08-15.Retrieved2023-08-15.
  49. ^abPetzold A, Solimena M, Knoch KP (October 2015)."Mechanisms of Beta Cell Dysfunction Associated With Viral Infection".Current Diabetes Reports(Review).15(10): 73.doi:10.1007/s11892-015-0654-x.PMC4539350.PMID26280364.So far, none of the hypotheses accounting for virus-induced beta cell autoimmunity has been supported by stringent evidence in humans, and the involvement of several mechanisms rather than just one is also plausible.
  50. ^Butalia S, Kaplan GG, Khokhar B, Rabi DM (December 2016). "Environmental Risk Factors and Type 1 Diabetes: Past, Present, and Future".Canadian Journal of Diabetes(Review).40(6): 586–593.doi:10.1016/j.jcjd.2016.05.002.PMID27545597.
  51. ^Laugesen E, Østergaard JA, Leslie RD (July 2015)."Latent autoimmune diabetes of the adult: current knowledge and uncertainty".Diabetic Medicine.32(7): 843–852.doi:10.1111/dme.12700.PMC4676295.PMID25601320.
  52. ^"What Is Diabetes?".Diabetes Daily.Archivedfrom the original on 2023-10-04.Retrieved2023-09-10.
  53. ^Nolasco-Rosales, Germán Alberto; Ramírez-González, Dania; Rodríguez-Sánchez, Ester; Ávila-Fernandez, Ángela; Villar-Juarez, Guillermo Efrén; González-Castro, Thelma Beatriz; Tovilla-Zárate, Carlos Alfonso; Guzmán-Priego, Crystell Guadalupe; Genis-Mendoza, Alma Delia; Ble-Castillo, Jorge Luis; Marín-Medina, Alejandro; Juárez-Rojop, Isela Esther (2023-04-29)."Identification and phenotypic characterization of patients with LADA in a population of southeast Mexico".Scientific Reports.13(1): 7029.Bibcode:2023NatSR..13.7029N.doi:10.1038/s41598-023-34171-2.ISSN2045-2322.PMC10148806.PMID37120620.
  54. ^Freeman, Andrew M.; Acevedo, Luis A.; Pennings, Nicholas (2024),"Insulin Resistance",StatPearls,Treasure Island (FL): StatPearls Publishing,PMID29939616,archivedfrom the original on 2024-02-07,retrieved2024-02-13
  55. ^American Diabetes Association (January 2017)."2. Classification and Diagnosis of Diabetes".Diabetes Care.40(Suppl 1): S11–S24.doi:10.2337/dc17-S005.PMID27979889.
  56. ^Carris NW, Magness RR, Labovitz AJ (February 2019)."Prevention of Diabetes Mellitus in Patients With Prediabetes".The American Journal of Cardiology.123(3): 507–512.doi:10.1016/j.amjcard.2018.10.032.PMC6350898.PMID30528418.
  57. ^abRisérus U, Willett WC, Hu FB (January 2009)."Dietary fats and prevention of type 2 diabetes".Progress in Lipid Research.48(1): 44–51.doi:10.1016/j.plipres.2008.10.002.PMC2654180.PMID19032965.
  58. ^Fletcher, Barbara; Gulanick, Meg; Lamendola, Cindy (January 2002)."Risk factors for type 2 diabetes mellitus".The Journal of Cardiovascular Nursing.16(2): 17–23.doi:10.1097/00005082-200201000-00003.ISSN0889-4655.PMID11800065.Archivedfrom the original on 2023-10-20.Retrieved2023-10-12.
  59. ^Malik VS, Popkin BM, Bray GA, Després JP, Hu FB (March 2010)."Sugar-sweetened beverages, obesity, type 2 diabetes mellitus, and cardiovascular disease risk".Circulation.121(11): 1356–1364.doi:10.1161/CIRCULATIONAHA.109.876185.PMC2862465.PMID20308626.
  60. ^Malik VS, Popkin BM, Bray GA, Després JP, Willett WC, Hu FB (November 2010)."Sugar-sweetened beverages and risk of metabolic syndrome and type 2 diabetes: a meta-analysis".Diabetes Care.33(11): 2477–2483.doi:10.2337/dc10-1079.PMC2963518.PMID20693348.
  61. ^Hu EA, Pan A, Malik V, Sun Q (March 2012)."White rice consumption and risk of type 2 diabetes: meta-analysis and systematic review".BMJ.344:e1454.doi:10.1136/bmj.e1454.PMC3307808.PMID22422870.
  62. ^Lee IM, Shiroma EJ, Lobelo F, Puska P, Blair SN, Katzmarzyk PT (July 2012)."Effect of physical inactivity on major non-communicable diseases worldwide: an analysis of burden of disease and life expectancy".Lancet.380(9838): 219–229.doi:10.1016/S0140-6736(12)61031-9.PMC3645500.PMID22818936.
  63. ^Huang H, Yan P, Shan Z, Chen S, Li M, Luo C, et al. (November 2015). "Adverse childhood experiences and risk of type 2 diabetes: A systematic review and meta-analysis".Metabolism.64(11): 1408–1418.doi:10.1016/j.metabol.2015.08.019.PMID26404480.
  64. ^Zhang Y, Liu Y, Su Y, You Y, Ma Y, Yang G, et al. (November 2017)."The metabolic side effects of 12 antipsychotic drugs used for the treatment of schizophrenia on glucose: a network meta-analysis".BMC Psychiatry.17(1): 373.doi:10.1186/s12888-017-1539-0.PMC5698995.PMID29162032.
  65. ^ab"National Diabetes Clearinghouse (NDIC): National Diabetes Statistics 2011".U.S. Department of Health and Human Services. Archived fromthe originalon 17 April 2014.Retrieved22 April2014.
  66. ^abSoldavini J (November 2019). "Krause's Food & The Nutrition Care Process".Journal of Nutrition Education and Behavior.51(10): 1225.doi:10.1016/j.jneb.2019.06.022.ISSN1499-4046.S2CID209272489.
  67. ^"Managing & Treating Gestational Diabetes | NIDDK".National Institute of Diabetes and Digestive and Kidney Diseases.Archivedfrom the original on 2019-05-06.Retrieved2019-05-06.
  68. ^Tarvonen M, Hovi P, Sainio S, Vuorela P, Andersson S, Teramo K (November 2021)."Intrapartal cardiotocographic patterns and hypoxia-related perinatal outcomes in pregnancies complicated by gestational diabetes mellitus".Acta Diabetologica.58(11): 1563–1573.doi:10.1007/s00592-021-01756-0.PMC8505288.PMID34151398.S2CID235487220.
  69. ^National Collaborating Centre for Women's and Children's Health (February 2015)."Intrapartum care".Diabetes in Pregnancy: Management of diabetes and its complications from preconception to the postnatal period.National Institute for Health and Care Excellence (UK).Archivedfrom the original on 2021-08-28.Retrieved2018-08-21.
  70. ^"Monogenic Forms of Diabetes".National institute of diabetes and digestive and kidney diseases.US NIH.Archivedfrom the original on 12 March 2017.Retrieved12 March2017.
  71. ^Thanabalasingham G, Owen KR (October 2011). "Diagnosis and management of maturity onset diabetes of the young (MODY)".BMJ.343(oct19 3): d6044.doi:10.1136/bmj.d6044.PMID22012810.S2CID44891167.
  72. ^ab"Definition, Diagnosis and Classification of Diabetes Mellitus and its Complications"(PDF).World Health Organization.1999.Archived(PDF)from the original on 2003-03-08.
  73. ^Cleland SJ, Fisher BM, Colhoun HM, Sattar N, Petrie JR (July 2013)."Insulin resistance in type 1 diabetes: what is 'double diabetes' and what are the risks?".Diabetologia.56(7). National Library of Medicine: 1462–1470.doi:10.1007/s00125-013-2904-2.PMC3671104.PMID23613085.
  74. ^Unless otherwise specified, reference is: Table 20-5 inMitchell, Richard Sheppard; Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson (2007).Robbins Basic Pathology(8th ed.). Philadelphia: Saunders.ISBN978-1-4160-2973-1.
  75. ^Sattar N, Preiss D, Murray HM, Welsh P, Buckley BM, de Craen AJ, et al. (February 2010). "Statins and risk of incident diabetes: a collaborative meta-analysis of randomised statin trials".Lancet.375(9716): 735–742.doi:10.1016/S0140-6736(09)61965-6.PMID20167359.S2CID11544414.
  76. ^Wilcox, Gisela (2005-05-05)."Insulin and Insulin Resistance".Clinical Biochemist Reviews.26(2): 19–39.ISSN0159-8090.PMC1204764.PMID16278749.
  77. ^"Insulin Basics".American Diabetes Association.Archivedfrom the original on 21 June 2023.Retrieved25 June2023.
  78. ^abcdShoback DG, Gardner D, eds. (2011).Greenspan's basic & clinical endocrinology(9th ed.). McGraw-Hill Medical.ISBN978-0-07-162243-1.
  79. ^Barrett KE, et al. (2012).Ganong's review of medical physiology(24th ed.). McGraw-Hill Medical.ISBN978-0-07-178003-2.
  80. ^Murray RK, et al. (2012).Harper's illustrated biochemistry(29th ed.). McGraw-Hill Medical.ISBN978-0-07-176576-3.
  81. ^Mogotlane S (2013).Juta's Complete Textbook of Medical Surgical Nursing.Cape Town: Juta. p. 839.
  82. ^"Summary of revisions for the 2010 Clinical Practice Recommendations".Diabetes Care.33(Suppl 1): S3. January 2010.doi:10.2337/dc10-S003.PMC2797388.PMID20042773.Archivedfrom the original on 13 January 2010.Retrieved29 January2010.
  83. ^Definition and diagnosis of diabetes mellitus and intermediate hyperglycemia: Report of a WHO/IDF consultation(PDF).Geneva:World Health Organization.2006. p. 21.ISBN978-92-4-159493-6.
  84. ^Vijan S (March 2010). "In the clinic. Type 2 diabetes".Annals of Internal Medicine.152(5): ITC31-15, quiz ITC316.doi:10.7326/0003-4819-152-5-201003020-01003.PMID20194231.
  85. ^Saydah SH, Miret M, Sung J, Varas C, Gause D, Brancati FL (August 2001)."Postchallenge hyperglycemia and mortality in a national sample of U.S. adults".Diabetes Care.24(8): 1397–1402.doi:10.2337/diacare.24.8.1397.PMID11473076.
  86. ^Definition and diagnosis of diabetes mellitus and intermediate hyperglycemia: report of a WHO/IDF consultation(PDF).World Health Organization. 2006. p. 21.ISBN978-92-4-159493-6.Archived(PDF)from the original on 11 May 2012.
  87. ^Santaguida PL, Balion C, Hunt D, Morrison K, Gerstein H, Raina P, et al. (August 2005)."Diagnosis, prognosis, and treatment of impaired glucose tolerance and impaired fasting glucose".Evidence Report/Technology Assessment(128).Agency for Healthcare Research and Quality:1–11.PMC4780988.PMID16194123.Archivedfrom the original on 16 September 2008.Retrieved20 July2008.
  88. ^Bartoli E, Fra GP, Carnevale Schianca GP (February 2011). "The oral glucose tolerance test (OGTT) revisited".European Journal of Internal Medicine.22(1): 8–12.doi:10.1016/j.ejim.2010.07.008.PMID21238885.
  89. ^Selvin E, Steffes MW, Zhu H, Matsushita K, Wagenknecht L, Pankow J, et al. (March 2010)."Glycated hemoglobin, diabetes, and cardiovascular risk in nondiabetic adults".The New England Journal of Medicine.362(9): 800–811.CiteSeerX10.1.1.589.1658.doi:10.1056/NEJMoa0908359.PMC2872990.PMID20200384.
  90. ^Jacobsen, Laura M.; Haller, Michael J.; Schatz, Desmond A. (2018-03-06)."Understanding Pre-Type 1 Diabetes: The Key to Prevention".Frontiers in Endocrinology.9:70.doi:10.3389/fendo.2018.00070.PMC5845548.PMID29559955.
  91. ^"Tackling risk factors for type 2 diabetes in adolescents: PRE-STARt study in Euskadi".Anales de Pediatria.95(3). Anales de Pediatría: 186–196. 2020.doi:10.1016/j.anpedi.2020.11.001.PMID33388268.
  92. ^Kyu HH, Bachman VF, Alexander LT, Mumford JE, Afshin A, Estep K, et al. (August 2016)."Physical activity and risk of breast cancer, colon cancer, diabetes, ischemic heart disease, and ischemic stroke events: systematic review and dose-response meta-analysis for the Global Burden of Disease Study 2013".BMJ.354:i3857.doi:10.1136/bmj.i3857.PMC4979358.PMID27510511.
  93. ^ab"Simple Steps to Preventing Diabetes".The Nutrition Source.Harvard T.H. Chan School of Public Health. 18 September 2012.Archivedfrom the original on 25 April 2014.
  94. ^Willi C, Bodenmann P, Ghali WA, Faris PD, Cornuz J (December 2007). "Active smoking and the risk of type 2 diabetes: a systematic review and meta-analysis".JAMA.298(22): 2654–2664.doi:10.1001/jama.298.22.2654.PMID18073361.S2CID30550981.
  95. ^"Chronic diseases and their common risk factors"(PDF).World Health Organization. 2005.Archived(PDF)from the original on 2016-10-17.Retrieved30 August2016.
  96. ^CDC (2023-07-31)."Diabetes and Your Immune System".Centers for Disease Control and Prevention.Retrieved2024-04-25.
  97. ^Singh, Awadhesh Kumar; Gupta, Ritesh; Ghosh, Amerta; Misra, Anoop (2020)."Diabetes in COVID-19: Prevalence, pathophysiology, prognosis and practical considerations".Diabetes & Metabolic Syndrome.14(4): 303–310.doi:10.1016/j.dsx.2020.04.004.ISSN1878-0334.PMC7195120.PMID32298981.
  98. ^Abdelhafiz, Ahmed H.; Emmerton, Demelza; Sinclair, Alan J. (July 2021)."Diabetes in COVID-19 pandemic-prevalence, patient characteristics and adverse outcomes".International Journal of Clinical Practice.75(7): e14112.doi:10.1111/ijcp.14112.ISSN1742-1241.PMC7995213.PMID33630378.
  99. ^"Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). UK Prospective Diabetes Study (UKPDS) Group".Lancet.352(9131): 837–853. 1998-09-12.doi:10.1016/S0140-6736(98)07019-6.ISSN0140-6736.PMID9742976.
  100. ^abcd"Managing diabetes".National Institute of Diabetes and Digestive and Kidney Diseases, US National Institutes of Health. 1 December 2016.Archivedfrom the original on 6 March 2023.Retrieved4 February2023.
  101. ^Toumpanakis A, Turnbull T, Alba-Barba I (2018-10-30)."Effectiveness of plant-based diets in promoting well-being in the management of type 2 diabetes: a systematic review".BMJ Open Diabetes Research & Care.6(1): e000534.doi:10.1136/bmjdrc-2018-000534.PMC6235058.PMID30487971.
  102. ^The Diabetes Control and Complications Trial Research Group (April 1995). "The effect of intensive diabetes therapy on the development and progression of neuropathy".Annals of Internal Medicine.122(8): 561–568.doi:10.7326/0003-4819-122-8-199504150-00001.PMID7887548.S2CID24754081.
  103. ^"The A1C test and diabetes".National Institute of Diabetes and Digestive and Kidney Diseases, US National Institutes of Health. 1 April 2018.Archivedfrom the original on 4 February 2023.Retrieved4 February2023.
  104. ^Qaseem A, Wilt TJ, Kansagara D, et al. (April 2018)."Hemoglobin A1c Targets for Glycemic Control With Pharmacologic Therapy for Nonpregnant Adults With Type 2 Diabetes Mellitus: A Guidance Statement Update From the American College of Physicians".Annals of Internal Medicine.168(8): 569–576.doi:10.7326/M17-0939.PMID29507945.
  105. ^National Institute for Health and Clinical Excellence.Clinical guideline 66: Type 2 diabetes.London, 2008.
  106. ^Bus SA, van Deursen RW, Armstrong DG, Lewis JE, Caravaggi CF, Cavanagh PR (January 2016)."Footwear and offloading interventions to prevent and heal foot ulcers and reduce plantar pressure in patients with diabetes: a systematic review".Diabetes/Metabolism Research and Reviews.32(Suppl 1): 99–118.doi:10.1002/dmrr.2702.PMID26342178.S2CID24862853.
  107. ^Heuch L, Streak Gomersall J (July 2016). "Effectiveness of offloading methods in preventing primary diabetic foot ulcers in adults with diabetes: a systematic review".JBI Database of Systematic Reviews and Implementation Reports.14(7): 236–265.doi:10.11124/JBISRIR-2016-003013.PMID27532798.S2CID12012686.
  108. ^van Netten JJ, Raspovic A, Lavery LA, Monteiro-Soares M, Rasmussen A, Sacco IC, Bus SA (March 2020)."Prevention of foot ulcers in the at-risk patient with diabetes: a systematic review"(PDF).Diabetes/Metabolism Research and Reviews.36(S1 Suppl 1): e3270.doi:10.1002/dmrr.3270.PMID31957213.S2CID210830578.Archived(PDF)from the original on 2023-02-09.Retrieved2023-01-23.
  109. ^Mayfield JA, Reiber GE, Sanders LJ, Janisse D, Pogach LM (January 2004)."Preventive foot care in diabetes".Diabetes Care.27(suppl_1): S63–S64.doi:10.2337/diacare.27.2007.S63.PMID14693928.
  110. ^McBain H, Mulligan K, Haddad M, Flood C, Jones J, Simpson A, et al. (Cochrane Metabolic and Endocrine Disorders Group) (April 2016)."Self management interventions for type 2 diabetes in adult people with severe mental illness".The Cochrane Database of Systematic Reviews.2016(4): CD011361.doi:10.1002/14651858.CD011361.pub2.PMC10201333.PMID27120555.
  111. ^Haw JS, Galaviz KI, Straus AN, et al. (December 2017)."Long-term Sustainability of Diabetes Prevention Approaches: A Systematic Review and Meta-analysis of Randomized Clinical Trials".JAMA Internal Medicine.177(12): 1808–1817.doi:10.1001/jamainternmed.2017.6040.PMC5820728.PMID29114778.
  112. ^Mottalib A, Kasetty M, Mar JY, Elseaidy T, Ashrafzadeh S, Hamdy O (August 2017)."Weight Management in Patients with Type 1 Diabetes and Obesity".Current Diabetes Reports.17(10): 92.doi:10.1007/s11892-017-0918-8.PMC5569154.PMID28836234.
  113. ^abAmerican Diabetes Association (January 2019)."5. Lifestyle Management:Standards of Medical Care in Diabetes-2019".Diabetes Care.42(Suppl 1): S46–S60.doi:10.2337/dc19-S005.PMID30559231.
  114. ^abcEvert AB, Dennison M, Gardner CD, et al. (May 2019)."Nutrition Therapy for Adults With Diabetes or Prediabetes: A Consensus Report".Diabetes Care(Professional society guidelines).42(5): 731–754.doi:10.2337/dci19-0014.PMC7011201.PMID31000505.
  115. ^abEmadian A, Andrews RC, England CY, Wallace V, Thompson JL (November 2015)."The effect of macronutrients on glycaemic control: a systematic review of dietary randomised controlled trials in overweight and obese adults with type 2 diabetes in which there was no difference in weight loss between treatment groups".The British Journal of Nutrition.114(10): 1656–1666.doi:10.1017/S0007114515003475.PMC4657029.PMID26411958.
  116. ^Grams J, Garvey WT (June 2015). "Weight Loss and the Prevention and Treatment of Type 2 Diabetes Using Lifestyle Therapy, Pharmacotherapy, and Bariatric Surgery: Mechanisms of Action".Current Obesity Reports.4(2): 287–302.doi:10.1007/s13679-015-0155-x.PMID26627223.S2CID207474124.
  117. ^abLohner, Szimonetta; Kuellenberg de Gaudry, Daniela; Toews, Ingrid; Ferenci, Tamas; Meerpohl, Joerg J (2020-05-25). Cochrane Metabolic and Endocrine Disorders Group (ed.)."Non-nutritive sweeteners for diabetes mellitus".Cochrane Database of Systematic Reviews.2020(5): CD012885.doi:10.1002/14651858.CD012885.pub2.PMC7387865.PMID32449201.
  118. ^Rosberger DF (December 2013). "Diabetic retinopathy: current concepts and emerging therapy".Endocrinology and Metabolism Clinics of North America.42(4): 721–745.doi:10.1016/j.ecl.2013.08.001.PMID24286948.
  119. ^MacIsaac RJ, Jerums G, Ekinci EI (March 2018). "Glycemic Control as Primary Prevention for Diabetic Kidney Disease".Advances in Chronic Kidney Disease.25(2): 141–148.doi:10.1053/j.ackd.2017.11.003.PMID29580578.
  120. ^Pozzilli P, Strollo R, Bonora E (March 2014)."One size does not fit all glycemic targets for type 2 diabetes".Journal of Diabetes Investigation.5(2): 134–141.doi:10.1111/jdi.12206.PMC4023573.PMID24843750.
  121. ^ab"Type 1 diabetes in adults: diagnosis and management".nice.org.uk.National Institute for Health and Care Excellence. 26 August 2015.Archivedfrom the original on 10 December 2020.Retrieved25 December2020.
  122. ^ab"Type 2 diabetes in adults: management".nice.org.uk.National Institute for Health and Care Excellence. 2 December 2015.Archivedfrom the original on 22 December 2020.Retrieved25 December2020.
  123. ^abKrentz AJ, Bailey CJ (2005). "Oral antidiabetic agents: current role in type 2 diabetes mellitus".Drugs.65(3): 385–411.doi:10.2165/00003495-200565030-00005.PMID15669880.S2CID29670619.
  124. ^Consumer Reports;American College of Physicians(April 2012),"Choosing a type 2 diabetes drug – Why the best first choice is often the oldest drug"(PDF),High Value Care,Consumer Reports,archived(PDF)from the original on July 2, 2014,retrievedAugust 14,2012
  125. ^Mitchell S, Malanda B, Damasceno A, et al. (September 2019)."A Roadmap on the Prevention of Cardiovascular Disease Among People Living With Diabetes".Global Heart.14(3): 215–240.doi:10.1016/j.gheart.2019.07.009.PMID31451236.
  126. ^Brunström M, Carlberg B (February 2016)."Effect of antihypertensive treatment at different blood pressure levels in patients with diabetes mellitus: systematic review and meta-analyses".BMJ.352:i717.doi:10.1136/bmj.i717.PMC4770818.PMID26920333.
  127. ^Brunström M, Carlberg B (September 2019)."Benefits and harms of lower blood pressure treatment targets: systematic review and meta-analysis of randomised placebo-controlled trials".BMJ Open.9(9): e026686.doi:10.1136/bmjopen-2018-026686.PMC6773352.PMID31575567.
  128. ^abcFox CS, Golden SH, Anderson C, et al. (September 2015)."Update on Prevention of Cardiovascular Disease in Adults With Type 2 Diabetes Mellitus in Light of Recent Evidence: A Scientific Statement From the American Heart Association and the American Diabetes Association".Diabetes Care.38(9): 1777–1803.doi:10.2337/dci15-0012.PMC4876675.PMID26246459.
  129. ^Cheng J, Zhang W, Zhang X, et al. (May 2014)."Effect of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers on all-cause mortality, cardiovascular deaths, and cardiovascular events in patients with diabetes mellitus: a meta-analysis".JAMA Internal Medicine.174(5): 773–785.doi:10.1001/jamainternmed.2014.348.PMID24687000.
  130. ^Zheng SL, Roddick AJ, Ayis S (September 2017)."Effects of aliskiren on mortality, cardiovascular outcomes and adverse events in patients with diabetes and cardiovascular disease or risk: A systematic review and meta-analysis of 13,395 patients".Diabetes & Vascular Disease Research.14(5): 400–406.doi:10.1177/1479164117715854.PMC5600262.PMID28844155.
  131. ^abCatalá-López F, Macías Saint-Gerons D, González-Bermejo D, et al. (March 2016)."Cardiovascular and Renal Outcomes of Renin-Angiotensin System Blockade in Adult Patients with Diabetes Mellitus: A Systematic Review with Network Meta-Analyses".PLOS Medicine.13(3): e1001971.doi:10.1371/journal.pmed.1001971.PMC4783064.PMID26954482.
  132. ^Pignone M, Alberts MJ, Colwell JA, et al. (June 2010)."Aspirin for primary prevention of cardiovascular events in people with diabetes: a position statement of the American Diabetes Association, a scientific statement of the American Heart Association, and an expert consensus document of the American College of Cardiology Foundation".Diabetes Care.33(6): 1395–1402.doi:10.2337/dc10-0555.PMC2875463.PMID20508233.
  133. ^Picot J, Jones J, Colquitt JL, Gospodarevskaya E, Loveman E, Baxter L, Clegg AJ (September 2009)."The clinical effectiveness and cost-effectiveness of bariatric (weight loss) surgery for obesity: a systematic review and economic evaluation".Health Technology Assessment.13(41): 1–190, 215–357, iii–iv.doi:10.3310/hta13410.hdl:10536/DRO/DU:30064294.PMID19726018.
  134. ^Frachetti KJ, Goldfine AB (April 2009)."Bariatric surgery for diabetes management".Current Opinion in Endocrinology, Diabetes and Obesity.16(2): 119–124.doi:10.1097/MED.0b013e32832912e7.PMID19276974.S2CID31797748.
  135. ^abSchulman AP, del Genio F, Sinha N, Rubino F (September–October 2009). ""Metabolic" surgery for treatment of type 2 diabetes mellitus ".Endocrine Practice.15(6): 624–631.doi:10.4158/EP09170.RAR.PMID19625245.
  136. ^Colucci RA (January 2011). "Bariatric surgery in patients with type 2 diabetes: a viable option".Postgraduate Medicine.123(1): 24–33.doi:10.3810/pgm.2011.01.2242.PMID21293081.S2CID207551737.
  137. ^Dixon JB, le Roux CW, Rubino F, Zimmet P (June 2012). "Bariatric surgery for type 2 diabetes".Lancet.379(9833): 2300–2311.doi:10.1016/S0140-6736(12)60401-2.PMID22683132.S2CID5198462.
  138. ^"Pancreas Transplantation".American Diabetes Association. Archived fromthe originalon 13 April 2014.Retrieved9 April2014.
  139. ^Sun J, Wang Y, Zhang X, Zhu S, He H (October 2020). "Prevalence of peripheral neuropathy in patients with diabetes: A systematic review and meta-analysis".Prim Care Diabetes.14(5): 435–444.doi:10.1016/j.pcd.2019.12.005.PMID31917119.
  140. ^Xu L, Sun Z, Casserly E, Nasr C, Cheng J, Xu J (June 2022)."Advances in Interventional Therapies for Painful Diabetic Neuropathy: A Systematic Review".Anesth Analg.134(6): 1215–1228.doi:10.1213/ANE.0000000000005860.PMC9124666.PMID35051958.
  141. ^abTu Y, Lineaweaver WC, Chen Z, Hu J, Mullins F, Zhang F (March 2017). "Surgical Decompression in the Treatment of Diabetic Peripheral Neuropathy: A Systematic Review and Meta-analysis".J Reconstr Microsurg.33(3): 151–157.doi:10.1055/s-0036-1594300.PMID27894152.
  142. ^Dellon AL (February 1988). "A cause for optimism in diabetic neuropathy".Ann Plast Surg.20(2): 103–5.doi:10.1097/00000637-198802000-00001.PMID3355053.
  143. ^abSessions J, Nickerson DS (March 2014)."Biologic Basis of Nerve Decompression Surgery for Focal Entrapments in Diabetic Peripheral Neuropathy".J Diabetes Sci Technol.8(2): 412–418.doi:10.1177/1932296814525030.PMC4455405.PMID24876595.
  144. ^Fadel ZT, Imran WM, Azhar T (August 2022)."Lower Extremity Nerve Decompression for Diabetic Peripheral Neuropathy: A Systematic Review and Meta-analysis".Plast Reconstr Surg Glob Open.10(8): e4478.doi:10.1097/GOX.0000000000004478.PMC9390809.PMID35999882.
  145. ^Xu L, Sun Z, Casserly E, Nasr C, Cheng J, Xu J (June 2022)."Advances in Interventional Therapies for Painful Diabetic Neuropathy: A Systematic Review".Anesth Analg.134(6): 1215–1228.doi:10.1213/ANE.0000000000005860.PMC9124666.PMID35051958.
  146. ^"Can social prescribing improve the health of people with diabetes?".National Institute for Health and Care Research – NIHR Evidence.2024.doi:10.3310/nihrevidence_61876.S2CID267264134.Archivedfrom the original on 26 January 2024.Retrieved26 January2024.
  147. ^Polisena J, Tran K, Cimon K, Hutton B, McGill S, Palmer K (October 2009). "Home telehealth for diabetes management: a systematic review and meta-analysis".Diabetes, Obesity & Metabolism.11(10): 913–930.doi:10.1111/j.1463-1326.2009.01057.x.PMID19531058.S2CID44260857.
  148. ^abPal K, Eastwood SV, Michie S, et al. (Cochrane Metabolic and Endocrine Disorders Group) (March 2013)."Computer-based diabetes self-management interventions for adults with type 2 diabetes mellitus".The Cochrane Database of Systematic Reviews.2013(3): CD008776.doi:10.1002/14651858.CD008776.pub2.PMC6486319.PMID23543567.
  149. ^Wei I, Pappas Y, Car J, Sheikh A, Majeed A, et al. (Cochrane Metabolic and Endocrine Disorders Group) (December 2011)."Computer-assisted versus oral-and-written dietary history taking for diabetes mellitus".The Cochrane Database of Systematic Reviews.2011(12): CD008488.doi:10.1002/14651858.CD008488.pub2.PMC6486022.PMID22161430.
  150. ^abcdeElflein J (10 December 2019).Estimated number diabetics worldwide.Archivedfrom the original on 29 July 2020.Retrieved17 May2020.
  151. ^Shi Y, Hu FB (June 2014). "The global implications of diabetes and cancer".Lancet.383(9933): 1947–1948.doi:10.1016/S0140-6736(14)60886-2.PMID24910221.S2CID7496891.
  152. ^abcdef"Global Report on Diabetes"(PDF).World Health Organization. 2016.Archived(PDF)from the original on 16 May 2018.Retrieved20 September2018.
  153. ^Gale EA, Gillespie KM (January 2001)."Diabetes and gender".Diabetologia.44(1): 3–15.doi:10.1007/s001250051573.PMID11206408.
  154. ^Meisinger C, Thorand B, Schneider A, Stieber J, Döring A, Löwel H (January 2002)."Sex differences in risk factors for incident type 2 diabetes mellitus: the MONICA Augsburg cohort study".Archives of Internal Medicine.162(1): 82–89.doi:10.1001/archinte.162.1.82.PMID11784224.
  155. ^"The top 10 causes of death Fact sheet N°310".World Health Organization. October 2013.Archivedfrom the original on 30 May 2017.
  156. ^Public Health Agency of Canada,Diabetes in Canada: Facts and figures from a public health perspective.Ottawa, 2011.
  157. ^Mathers CD, Loncar D (November 2006)."Projections of global mortality and burden of disease from 2002 to 2030".PLOS Medicine.3(11): e442.doi:10.1371/journal.pmed.0030442.PMC1664601.PMID17132052.
  158. ^abWild S, Roglic G, Green A, Sicree R, King H (May 2004)."Global prevalence of diabetes: estimates for the year 2000 and projections for 2030".Diabetes Care.27(5): 1047–1053.doi:10.2337/diacare.27.5.1047.PMID15111519.
  159. ^"Prevalence of Prediabetes Among Adults – Diabetes".CDC.2018-03-13.Archivedfrom the original on 2023-03-06.Retrieved2022-12-15.
  160. ^Ripoll BC, Leutholtz I (2011-04-25).Exercise and disease management(2nd ed.). Boca Raton: CRC Press. p. 25.ISBN978-1-4398-2759-8.Archivedfrom the original on 2016-04-03.
  161. ^abcdefghPoretsky L, ed. (2009).Principles of diabetes mellitus(2nd ed.). New York: Springer. p. 3.ISBN978-0-387-09840-1.Archivedfrom the original on 2016-04-04.
  162. ^abRoberts J (2015)."Sickening sweet".Distillations.Vol. 1, no. 4. pp. 12–15.Archivedfrom the original on 13 November 2019.Retrieved20 March2018.
  163. ^abLaios K, Karamanou M, Saridaki Z, Androutsos G (2012)."Aretaeus of Cappadocia and the first description of diabetes"(PDF).Hormones.11(1): 109–113.doi:10.1007/BF03401545.PMID22450352.S2CID4730719.Archived(PDF)from the original on 2017-01-04.
  164. ^abOxford English Dictionary.diabetes.Retrieved 2011-06-10.
  165. ^abHarper D (2001–2010)."Online Etymology Dictionary.diabetes.".Archivedfrom the original on 2012-01-13.Retrieved2011-06-10.
  166. ^Aretaeus,De causis et signis acutorum morborum (lib. 2),Κεφ. β. περὶ Διαβήτεω (Chapter 2,On Diabetes,Greek original)Archived2014-07-02 at theWayback Machine,on Perseus
  167. ^abcdOxford English Dictionary.mellite.Retrieved 2011-06-10.
  168. ^abcd"MyEtimology.mellitus.".Archived from the original on 2011-03-16.Retrieved2011-06-10.{{cite web}}:CS1 maint: unfit URL (link)
  169. ^Oxford English Dictionary.-ite.Retrieved 2011-06-10.
  170. ^Guthrie, Diana W. (1988)."Diabetes Urine Testing: An Historical Perspective".The Diabetes Educator.14(6): 521–525.doi:10.1177/014572178801400615.PMID3061764.
  171. ^Tulchinsky TH, Varavikova EA (2008).The New Public Health, Second Edition.New York:Academic Press.p. 200.ISBN978-0-12-370890-8.
  172. ^Piwernetz K, Home PD, Snorgaard O, Antsiferov M, Staehr-Johansen K, Krans M (May 1993). "Monitoring the targets of the St Vincent Declaration and the implementation of quality management in diabetes care: the DIABCARE initiative. The DIABCARE Monitoring Group of the St Vincent Declaration Steering Committee".Diabetic Medicine.10(4): 371–377.doi:10.1111/j.1464-5491.1993.tb00083.x.PMID8508624.S2CID9931183.
  173. ^Dubois H, Bankauskaite V (2005)."Type 2 diabetes programmes in Europe"(PDF).Euro Observer.7(2): 5–6.Archived(PDF)from the original on 2012-10-24.
  174. ^CDC (2022-11-03)."Diabetes Stigma: Learn About It, Recognize It, Reduce It".Centers for Disease Control and Prevention.Archivedfrom the original on 2023-10-31.Retrieved2023-10-31.
  175. ^Schabert, Jasmin; Browne, Jessica L.; Mosely, Kylie; Speight, Jane (2013-03-01)."Social Stigma in Diabetes".The Patient – Patient-Centered Outcomes Research.6(1): 1–10.doi:10.1007/s40271-012-0001-0.ISSN1178-1661.PMID23322536.S2CID207490680.
  176. ^Puhl, Rebecca M.; Himmelstein, Mary S.; Hateley-Browne, Jessica L.; Speight, Jane (October 2020)."Weight stigma and diabetes stigma in U.S. adults with type 2 diabetes: Associations with diabetes self-care behaviors and perceptions of health care".Diabetes Research and Clinical Practice.168:108387.doi:10.1016/j.diabres.2020.108387.ISSN0168-8227.PMID32858100.S2CID221366068.
  177. ^Spanakis, Elias K.; Golden, Sherita Hill (December 2013)."Race/Ethnic Difference in Diabetes and Diabetic Complications".Current Diabetes Reports.13(6): 10.1007/s11892–013–0421–9.doi:10.1007/s11892-013-0421-9.ISSN1534-4827.PMC3830901.PMID24037313.
  178. ^CDC (2022-04-04)."Hispanic/Latino Americans and Type 2 Diabetes".Centers for Disease Control and Prevention.Archivedfrom the original on 2023-10-31.Retrieved2023-10-31.
  179. ^CDC (2022-11-21)."Diabetes and Asian American People".Centers for Disease Control and Prevention.Archivedfrom the original on 2023-10-31.Retrieved2023-10-31.
  180. ^Stewart WF, Ricci JA, Chee E, Hirsch AG, Brandenburg NA (June 2007). "Lost productive time and costs due to diabetes and diabetic neuropathic pain in the US workforce".Journal of Occupational and Environmental Medicine.49(6): 672–679.doi:10.1097/JOM.0b013e318065b83a.PMID17563611.S2CID21487348.
  181. ^Washington R.E.; Andrews R.M.; Mutter R.L. (November 2013)."Emergency Department Visits for Adults with Diabetes, 2010".HCUP Statistical Brief(167). Rockville MD: Agency for Healthcare Research and Quality.PMID24455787.Archivedfrom the original on 2013-12-03.
  182. ^"Type 1 vs. Type 2 Diabetes Differences: Which One Is Worse?".MedicineNet.Archivedfrom the original on 2021-04-14.Retrieved2021-03-21.
  183. ^Parker K (2008).Living with diabetes.New York: Facts On File. p.143.ISBN978-1-4381-2108-6.
  184. ^Niaz K, Maqbool F, Khan F, Hassan FI, Momtaz S, Abdollahi M (April 2018)."Comparative occurrence of diabetes in canine, feline, and few wild animals and their association with pancreatic diseases and ketoacidosis with therapeutic approach".Veterinary World.11(4): 410–422.doi:10.14202/vetworld.2018.410-422.PMC5960778.PMID29805204.
  185. ^Stahl SJ (2006-01-01). "Hyperglycemia in Reptiles". In Mader DR (ed.).Reptile Medicine and Surgery(Second ed.). Saint Louis: W.B. Saunders. pp. 822–830.doi:10.1016/b0-72-169327-x/50062-6.ISBN978-0-7216-9327-9.
  186. ^Sweazea KL (8 July 2022). "Revisiting glucose regulation in birds - A negative model of diabetes complications".Comparative Biochemistry and Physiology. Part B, Biochemistry & Molecular Biology.262:110778.doi:10.1016/j.cbpb.2022.110778.PMID35817273.S2CID250404382.
  187. ^ab"Diabetes mellitus".Merck Veterinary Manual(9th ed.). 2005.Archivedfrom the original on 2011-09-27.Retrieved2011-10-23.
  188. ^Öhlund M.Feline diabetes mellitus Aspects on epidemiology and pathogenesis(PDF).Acta Universitatis agriculturae Sueciae.ISBN978-91-7760-067-1.Archived(PDF)from the original on 2021-04-13.Retrieved2017-12-18.
edit