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Not to be confused withThymine.

Thiamine
Skeletal formula and ball-and-stick model of the thiaminecation
Clinical data
Pronunciation/ˈθaɪ.əmɪn/THY-ə-min
Other namesVitamin B1,aneurine, thiamin
AHFS/Drugs.comMonograph
License data
Routes of
administration		by mouth, IV, IM[1]
Drug classvitamin
ATC code
Legal status
Legal status
Pharmacokineticdata
Bioavailability3.7% to 5.3% (Thiamine hydrochloride)[2]
Identifiers
  • 2-[3-[(4-amino-2-methylpyrimidin-5-yl)methyl]-4-methyl-1,3-thiazol-3-ium-5-yl]ethanol
CAS Number
PubChemCID
DrugBank
ChemSpider
UNII
KEGG
ChEBI
ChEMBL
CompTox Dashboard(EPA)
Chemical and physical data
FormulaC12H17N4OS+
Molar mass265.36g·mol−1
3D model (JSmol)
  • cation: Cc2ncc(C[n+]1csc(CCO)c1C)c(N)n2
  • cation: InChI=1S/C12H17N4OS/c1-8-11(3-4-17)18-7-16(8)6-10-5-14-9(2)15-12(10)13/h5,7,17H,3-4,6H2,1-2H3,(H2,13,14,15)/q+1checkY
  • Key:JZRWCGZRTZMZEH-UHFFFAOYSA-N

Thiamine,also known asthiaminandvitamin B1,is avitamin,anessential micronutrientfor humans and animals.[3][4]It is found in food and commercially synthesized to be adietary supplementormedication.[1][5]Phosphorylatedforms of thiamine are required for somemetabolic reactions,including the breakdown ofglucoseandamino acids.[1]

Food sources of thiamine includewhole grains,legumes,and some meats and fish.[1][6]Grain processingremoves much of the vitamin content, so in many countriescerealsandfloursareenrichedwith thiamine.[1]Supplements and medications are available to treat and preventthiamine deficiencyand the disorders that result from it such asberiberiandWernicke encephalopathy.They are also used to treatmaple syrup urine diseaseandLeigh syndrome.Supplements and medications are typically takenby mouth,but may also be given byintravenousorintramuscular injection.[7]

Thiamine supplements are generally well tolerated.Allergic reactions,includinganaphylaxis,may occur when repeated doses are given by injection.[7][8]Thiamine is on theWorld Health Organization's List of Essential Medicines.[9]It is available as ageneric medication,and in some countries as a non-prescription dietary supplement.[7]

Definition

[edit]

Thiamine is one of theB vitaminsand is also known as vitamin B1.[3][4]It is acationthat is usually supplied as achloridesalt.It issolublein water,methanolandglycerol,but practically insoluble in less polarorganic solvents.[10][11]In the body, thiamine can formderivatives;the most well-characterized of which isthiamine pyrophosphate(TPP), acoenzymein thecatabolismof sugars and amino acids.[3]

The chemical structure consists of anaminopyrimidineand athiazoliumring linked by amethylene bridge.The thiazole is substituted with methyl andhydroxyethyl side chains.Thiamine is stable at acidicpH,but it is unstable inalkaline solutionsand from exposure toheat.[10][11]It reacts strongly inMaillard-type reactions.[10]Oxidationyields the fluorescent derivativethiochrome,which can be used to determine the amount of the vitamin present in biological samples.[12]

Deficiency

[edit]
Main article:Thiamine deficiency

Well-known disorders caused by thiamine deficiency includeberiberi,Wernicke–Korsakoff syndrome,optic neuropathy,Leigh's disease,African seasonalataxia(or Nigerian seasonal ataxia), andcentral pontine myelinolysis.[13]Symptoms includemalaise,weight loss, irritability and confusion.[10][14][15]

In Western countries, chronic alcoholism is a risk factor for deficiency. Also at risk are older adults, persons withHIV/AIDSordiabetes,and those who have hadbariatric surgery.[1]Varying degrees of thiamine insufficiency have been associated with the long-term use ofdiuretics.[16][17]

Biological functions

[edit]
Thiamine monophosphate (ThMP)

Five natural thiamine phosphate derivatives are known:thiamine monophosphate(ThMP), thiamine pyrophosphate (TPP),thiamine triphosphate(ThTP),adenosine thiamine diphosphate(AThDP) andadenosine thiamine triphosphate(AThTP). They are involved in many cellular processes.[18]The best-characterized form is TPP, acoenzymein thecatabolismof sugars and amino acids. While its role is well-known, the non-coenzyme action of thiamine and derivatives may be realized through binding to proteins which do not use that mechanism.[19]No physiological role is known for the monophosphate except as an intermediate in cellular conversion of thiamine to the di- and triphosphates.[20]

Thiamine pyrophosphate

[edit]
Main article:thiamine pyrophosphate
Thiamine pyrophosphate (TPP)
The ylide form of TPP

Thiamine pyrophosphate (TPP), also called thiamine diphosphate (ThDP), participates as a coenzyme in metabolic reactions, including those in whichpolarity inversiontakes place.[21]Its synthesis is catalyzed by the enzymethiamine diphosphokinaseaccording to the reaction thiamine + ATP → TPP + AMP (EC 2.7.6.2). TPP is acoenzymefor several enzymes that catalyze the transfer of two-carbon units and in particular thedehydrogenation(decarboxylationand subsequent conjugation withcoenzyme A) of 2-oxoacids (alpha-keto acids). The mechanism of action of TPP as a coenzyme relies on its ability to form anylide.[22]Examples include:

The enzymes transketolase, pyruvate dehydrogenase (PDH), and 2-oxoglutarate dehydrogenase (OGDH) are important incarbohydrate metabolism.PDH links glycolysis to thecitric acid cycle.OGDH catalyzes the overall conversion of2-oxoglutarate(alpha-ketoglutarate) tosuccinyl-CoAand CO2during thecitric acid cycle.The reaction catalyzed by OGDH is a rate-limiting step in the citric acid cycle. The cytosolic enzyme transketolase is central to thepentose phosphate pathway,a major route for the biosynthesis of the pentosesugarsdeoxyriboseandribose.The mitochondrial PDH and OGDH are part of biochemical pathways that result in the generation ofadenosine triphosphate(ATP), which is the main energy transfer molecule for the cell. In the nervous system, PDH is also involved in the synthesis ofmyelinand the neurotransmitteracetylcholine.[11]

Thiamine triphosphate

[edit]
Thiamine triphosphate (ThTP)

ThTP is implicated inchloride channelactivation in the neurons of mammals and other animals, although its role is not well understood.[20]ThTP has been found in bacteria, fungi and plants, suggesting that it has other cellular roles.[23]InEscherichia coli,it is implicated in the response to amino acid starvation.[24]

Adenosine derivatives

[edit]
Adenosine thiamine diphosphate (AThDP)
Adenosine thiamine triphosphate (AThTP)

AThDP exists in small amounts in vertebrate liver, but its role remains unknown.[24]

AThTP is present inE. coli,where it accumulates as a result of carbon starvation. In this bacterium, AThTP may account for up to20% of total thiamine. It also exists in lesser amounts inyeast,roots of higher plants and animal tissue.[24]

Medical uses

[edit]
See also:Prenatal vitamins

During pregnancy, thiamine is sent to thefetusvia theplacenta.Pregnant women have a greater requirement for the vitamin than other adults, especially during thethird trimester.Pregnant women withhyperemesis gravidarumare at an increased risk of thiamine deficiency due to losses when vomiting.[25]Inlactatingwomen, thiamine is delivered in breast milk even if it results in thiamine deficiency in the mother.[4][26]

Thiamine is important not only formitochondrial membranedevelopment, but also forsynaptic membranefunction.[27]It has also been suggested that a deficiency hinders brain development in infants and may be a cause ofsudden infant death syndrome.[20]

Dietary recommendations

[edit]
US National Academy of Medicine
Age group RDA (mg/day)
Infants 0–6 months 0.2*
Infants 6–12 months 0.3*
1–3 years 0.5
4–8 years 0.6
9–13 years 0.9
Females 14–18 years 1.0
Males 14+ years 1.2
Females 19+ years 1.1
Pregnant/lactating females 14–50 1.4
* Adequate intake for infants, as an RDA has yet to be established[4]
European Food Safety Authority
Age group Adequate intake
(mg/MJ)[28]
All persons 7 months+ 0.1
Neither the US National Academy of Medicine nor the European Food Safety Authority have determined the tolerable upper intake level for thiamine[4]

TheUS National Academy of Medicineupdated the Estimated Average Requirements (EARs) andRecommended Dietary Allowances(RDAs) for thiamine in 1998. The EARs for thiamine for women and men aged 14 and over are 0.9 mg/day and 1.1 mg/day, respectively; the RDAs are 1.1 and 1.2 mg/day, respectively. RDAs are higher than EARs to provide adequate intake levels for individuals with higher than average requirements. The RDA during pregnancy and for lactating females is 1.4 mg/day. For infants up to the age of 12 months, the Adequate Intake (AI) is 0.2–0.3 mg/day and for children aged 1–13 years the RDA increases with age from 0.5 to 0.9 mg/day.[4]

TheEuropean Food Safety Authority(EFSA) refers to the collective set of information asDietary Reference Values,with Population Reference Intakes (PRIs) instead of RDAs, and Average Requirements instead of EARs. For women (including those pregnant or lactating), men and children the PRI is 0.1 mg thiamine per megajoule (MJ) of energy in their diet. As the conversion is 1 MJ = 239 kcal, an adult consuming 2390 kilocalories ought to be consuming 1.0 mg thiamine. This is slightly lower than the US RDA.[29]

Neither the National Academy of Medicine nor EFSA have set an upper intake level for thiamine, as there is no human data for adverse effects from high doses.[4][28]

Safety

[edit]

Thiamine is generally well tolerated and non-toxic whenadministered orally.[7]There are rare reports of adverse side effects when thiamine is givenintravenously,including allergic reactions,nausea,lethargy,andimpaired coordination.[28][3]

Labeling

[edit]

For US food and dietary supplement labeling purposes, the amount in a serving is expressed as a percent of Daily Value. Since May 27, 2016, the Daily Value has been 1.2 mg, in line with the RDA.[30][31]

Sources

[edit]

Thiamine is found in a wide variety of processed and whole foods,[18]includinglentils,peas,whole grains,pork,andnuts.[6][32]A typical daily prenatal vitamin product contains around 1.5 mg of thiamine.[33]

Food fortification

[edit]
Main article:Food fortification

Some countries require or recommend fortification of grain foods such aswheat,riceormaize(corn) because processing lowers vitamin content.[34]As of February 2022, 59 countries, mostly in North and Sub-Saharan Africa, require food fortification of wheat, rice or maize with thiamine or thiamine mononitrate. The amounts stipulated range from 2.0 to 10.0 mg/kg.[35]An additional 18 countries have a voluntary fortification program. For example, theIndian governmentrecommends 3.5 mg/kg for"maida" (white)and"atta" (whole wheat)flour.[36]

Synthesis

[edit]

Biosynthesis

[edit]

Thiamine biosynthesis occurs in bacteria, some protozoans, plants, and fungi.[37][38]Thethiazoleandpyrimidinemoieties are biosynthesized separately and are then combined to form ThMP by the action ofthiamine-phosphate synthase.

The pyrimidine ring system is formed in a reaction catalysed byphosphomethylpyrimidine synthase(ThiC), an enzyme in theradical SAMsuperfamily ofiron–sulfur proteins,which useS-adenosyl methionineas acofactor.[39][40]

The starting material is5-aminoimidazole ribotide,which undergoes arearrangement reactionviaradicalintermediates which incorporate the blue, green and red fragments shown into the product.[41][42]

The thiazole ring is formed in a reaction catalysed bythiazole synthase(EC 2.8.1.10).[39]The ultimate precursors are 1-deoxy-D-xylulose 5-phosphate, 2-iminoacetate and asulfur carrier proteincalled ThiS. An additional protein, ThiG, is also required to bring together all the components of the ring at the enzyme active site.[43]

A 3D representation of theTPP riboswitchwith thiamine bound

The final step to form ThMP involvesdecarboxylationof the thiazole intermediate, which reacts with thepyrophosphatederivative of phosphomethylpyrimidine, itself a product of akinase,phosphomethylpyrimidine kinase.[39]

The biosynthetic pathways differ among organisms. InE. coliand otherenterobacteriaceae,ThMP is phosphorylated to the cofactor TPP by athiamine-phosphate kinase(ThMP + ATP → TPP + ADP).[39]In most bacteria and ineukaryotes,ThMP is hydrolyzed to thiamine and then pyrophosphorylated to TPP bythiamine diphosphokinase(thiamine + ATP → TPP + AMP).[44]

The biosynthetic pathways are regulated byriboswitches.[3]If there is sufficient thiamine present in the cell then the thiamine binds to themRNAsfor the enzymes that are required in the pathway and prevents theirtranslation.If there is no thiamine present then there is no inhibition, and the enzymes required for the biosynthesis are produced. The specific riboswitch, theTPP riboswitch,is the only known riboswitch found in both eukaryotic andprokaryoticorganisms.[45]

Laboratory synthesis

[edit]

In the firsttotal synthesisin 1936, ethyl 3-ethoxypropanoate was treated withethyl formateto give an intermediate dicarbonyl compound which when reacted withacetamidineformed a substitutedpyrimidine.Conversion of its hydroxyl group to an amino group was carried out bynucleophilic aromatic substitution,first to the chloride derivative usingphosphorus oxychloride,followed by treatment withammonia.Theethoxygroup was then converted to a bromo derivative usinghydrobromic acid.In the final stage, thiamine (as its dibromide salt) was formed in analkylationreaction using 4-methyl-5-(2-hydroxyethyl)thiazole.[46]: 7 [47]

Industrial synthesis

[edit]
Diamine used in the manufacture of thiamine

Merck & Co.adapted the 1936 laboratory-scale synthesis, allowing them to manufacture thiamine inRahwayin 1937.[47]However, an alternative route using the intermediate Grewediamine(5-(aminomethyl)-2-methyl-4-pyrimidinamine), first published in 1937,[48]was investigated byHoffman La Rocheand competitive manufacturing processes followed. Efficient routes to the diamine have continued to be of interest.[47][49]In theEuropean Economic Area,thiamine is registered underREACH regulationand between 100 and 1,000 tonnes per annum are manufactured or imported there.[50]

Synthetic analogues

[edit]

Manyvitamin B1analogues,such asBenfotiamine,fursultiamine,andsulbutiamine,are synthetic derivatives of thiamine. Most were developed in Japan in the 1950s and 1960s as forms that were intended to improve absorption compared to thiamine.[51]Some are approved for use in some countries as a drug or non-prescription dietary supplement for treatment ofdiabetic neuropathyor other health conditions.[52][53][54]

Absorption, metabolism and excretion

[edit]

In the upper small intestine, thiamine phosphate esters present in food are hydrolyzed by alkalinephosphataseenzymes. At low concentrations, the absorption process is carrier-mediated. At higher concentrations, absorption also occurs viapassive diffusion.[3]Active transport can be inhibited by alcohol consumption or byfolate deficiency.[10]

The majority of thiamine inserumis bound to proteins, mainlyalbumin.Approximately90% of total thiamine in blood is inerythrocytes.A specific binding protein called thiamine-binding protein has been identified in rat serum and is believed to be a hormone-regulated carrier protein important for tissue distribution of thiamine.[14]Uptake of thiamine by cells of the blood and other tissues occurs via active transport and passive diffusion.[10]Two members of the family of transporter proteins encoded by the genesSLC19A2andSLC19A3are capable of thiamine transport.[20]In some tissues, thiamine uptake and secretion appear to be mediated by a Na+-dependent transporter and a transcellular proton gradient.[14]

Human storage of thiamine is about 25 to 30 mg, with the greatest concentrations in skeletal muscle, heart, brain, liver, and kidneys. ThMP and free (unphosphorylated) thiamine are present in plasma, milk,cerebrospinal fluid,and, it is presumed, allextracellular fluid.Unlike the highly phosphorylated forms of thiamine, ThMP and free thiamine are capable of crossing cell membranes. Calcium and magnesium have been shown to affect the distribution of thiamine in the body andmagnesium deficiencyhas been shown to aggravate thiamine deficiency.[20]Thiamine contents in human tissues are less than those of other species.[14][55]

Thiamine and its metabolites (2-methyl-4-amino-5-pyrimidine carboxylic acid, 4-methyl-thiazole-5-acetic acid, and others) are excreted principally in the urine.[3]

Interference

[edit]

Thebioavailabilityof thiamine in foods can be interfered with in a variety of ways.Sulfites,added to foods as a preservative,[56]will attack thiamine at the methylene bridge, cleaving the pyrimidine ring from the thiazole ring. The rate of this reaction is increased under acidic conditions.[14]Thiamine is degraded by thermolabilethiaminasespresent in some species of fish, shellfish and other foods.[10]The pupae of an African silk worm,Anaphe venata,is a traditional food in Nigeria. Consumption leads to thiamine deficiency.[57]Older literature reported that in Thailand, consumption of fermented, uncooked fish caused thiamine deficiency, but either abstaining from eating the fish or heating it first reversed the deficiency.[58]In ruminants, intestinal bacteria synthesize thiamine and thiaminases. The bacterial thiaminases are cell surface enzymes that must dissociate from the cell membrane before being activated; the dissociation can occur in ruminants underacidotic conditions.Indairy cows,over-feeding with grain causes subacute ruminal acidosis and increased ruminal bacteria thiaminase release, resulting in thiamine deficiency.[59]

From reports on two small studies conducted in Thailand, chewing slices ofareca nutwrapped inbetelleaves and chewing tea leaves reduced food thiamine bioavailability by a mechanism that may involvetannins.[58][60]

Bariatric surgery for weight loss is known to interfere with vitamin absorption.[61]A meta-analysis reported that27% of people who underwent bariatric surgeries experience vitamin B1deficiency.[62]

History

[edit]
Further information:Vitamin § History

Thiamine was the first of the water-soluble vitamins to be isolated.[63]The earliest observations in humans and in chickens had shown that diets of primarily polished white rice caused beriberi, but did not attribute it to the absence of a previously unknown essential nutrient.[64][65]

In 1884,Takaki Kanehiro,a surgeon general in theImperial Japanese Navy,rejected the previousgerm theoryfor beriberi and suggested instead that the disease was due to insufficiencies in the diet.[64]Switching diets on a navy ship, he discovered that replacing a diet of white rice only with one also containing barley, meat, milk, bread, and vegetables, nearly eliminated beriberi on a nine-month sea voyage. However, Takaki had added many foods to the successful diet and he incorrectly attributed the benefit to increased protein intake, as vitamins were unknown at the time. The Navy was not convinced of the need for such an expensive program of dietary improvement, and many men continued to die of beriberi, even during theRusso-Japanese warof 1904–5. Not until 1905, after the anti-beriberi factor had been discovered inrice bran(removed bypolishing into white rice) and in barley bran, was Takaki's experiment rewarded. He was made a baron in the Japanese peerage system, after which he was affectionately called "Barley Baron".[64]

The specific connection to grain was made in 1897 byChristiaan Eijkman,a military doctor in theDutch East Indies,who discovered that fowl fed on a diet of cooked, polished rice developed paralysis that could be reversed by discontinuing rice polishing.[65]He attributed beriberi to the high levels ofstarchin rice being toxic. He believed that the toxicity was countered in a compound present in the rice polishings.[66]An associate,Gerrit Grijns,correctly interpreted the connection between excessive consumption of polished rice and beriberi in 1901: He concluded that rice contains an essential nutrient in the outer layers of the grain that is removed by polishing.[67]Eijkman was eventually awarded theNobel Prize in Physiology and Medicinein 1929, because his observations led to the discovery of vitamins.

In 1910, a Japanese agricultural chemist ofTokyo Imperial University,Umetaro Suzuki,isolated a water-soluble thiamine compound from rice bran, which he namedaberic acid.(He later renamed itOrizanin.) He described the compound as not only an anti-beriberi factor, but also as being essential to human nutrition; however, this finding failed to gain publicity outside of Japan, because a claim that the compound was a new finding was omitted in translation of his publication from Japanese to German.[63]In 1911 a Polish biochemistCasimir Funkisolated theantineuriticsubstance from rice bran (the modern thiamine) that he called a "vitamine" (on account of its containing an amino group).[68][69]However, Funk did not completely characterize its chemical structure. Dutch chemists,Barend Coenraad Petrus Jansenand his closest collaborator Willem Frederik Donath, went on to isolate and crystallize the active agent in 1926,[70]whose structure was determined byRobert Runnels Williams,in 1934. Thiamine was named by the Williams team as aportmanteauof "thio" (meaning sulfur-containing) and "vitamin". The term "vitamin" coming indirectly, by way of Funk, from the amine group of thiamine itself (although by this time, vitamins were known to not always be amines, for example,vitamin C). Thiamine was also synthesized by the Williams group in 1936.[71]

SirRudolph Peters,inOxford,used pigeons to understand how thiamine deficiency results in the pathological-physiological symptoms of beriberi. Pigeons fed exclusively on polished rice developedopisthotonos,a condition characterized by head retraction. If not treated, the animals died after a few days. Administration of thiamine after opisthotonos was observed led to a complete cure within 30 minutes. As no morphological modifications were seen in the brain of the pigeons before and after treatment with thiamine, Peters introduced the concept of a biochemical-induced injury.[72]In 1937, Lohmann and Schuster showed that the diphosphorylated thiamine derivative, TPP, was a cofactor required for the oxidative decarboxylation of pyruvate.[73]

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[edit]
  • "Thiamine".Drug Information Portal.US National Library of Medicine.
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