Blood lipids
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Blood lipids(orblood fats) arelipidsin theblood,either free or bound to othermolecules.They are mostly transported in aphospholipid capsule,and the type of protein embedded in this outer shell determines the fate of the particle and its influence onmetabolism.Examples of these lipids includecholesterolandtriglycerides.The concentration of blood lipids depends on intake andexcretionfrom theintestine,and uptake andsecretionfromcells.Hyperlipidemiais the presence of elevated or abnormal levels oflipidsand/orlipoproteinsin theblood,and is a major risk factor forcardiovascular disease.
Fatty acids[edit]
Intestine intake[edit]
Short-andmedium chain fatty acidsare absorbed directly into the blood viaintestine capillariesand travel through theportal vein.Long-chain fatty acids,on the other hand, are too large to be directly released into the tiny intestine capillaries. Instead they are coated with a membrane composed ofphospholipidsandproteins,forming a large transporter particle calledchylomicron.The chylomicron enters alymphaticcapillary, then it is transported into the bloodstream at the leftsubclavian vein(having bypassed the liver).
In any case, the concentration of blood fatty acids increase temporarily after a meal.
Cell uptake[edit]
After a meal, when the blood concentration of fatty acids rises, there is an increase in uptake of fatty acids in different cells of the body, mainlyliver cells,adipocytesandmuscle cells.This uptake is stimulated byinsulinfrom thepancreas.As a result, the blood concentration of fatty acid stabilizes again after a meal.
Cell secretion[edit]
After a meal, some of the fatty acids taken up by the liver is converted intovery low density lipoproteins(VLDL) and again secreted into the blood.[1]
In addition, when a long time has passed since the last meal, the concentration of fatty acids in the blood decreases, which triggersadipocytesto release stored fatty acids into the blood asfree fatty acids,in order to supply e.g. muscle cells with energy.
In any case, also the fatty acids secreted from cells are anew taken up by other cells in the body, until enteringfatty acid metabolism[clarification needed].
Cholesterol[edit]
The fate of cholesterol in the blood is highly determined by its constitution oflipoproteins,where some types favour transport towards body tissues and others towards the liver for excretion into the intestines.
The 1987 report ofNational Cholesterol Education Program,Adult Treatment Panels suggest the totalblood cholesterol levelshould be: <200 mg/dl normal blood cholesterol, 200–239 mg/dl borderline-high, >240 mg/dl high cholesterol.[2]
The average amount ofblood cholesterolvaries with age, typically rising gradually until one is about 60 years old. There appear to be seasonal variations in cholesterol levels in humans, more, on average, in winter.[3]These seasonal variations seem to be inversely linked tovitamin Cintake.[4][5]
Intestine intake[edit]
Inlipid digestion,cholesterol is packed intochylomicronsin thesmall intestine,which are delivered to theportal veinandlymph.The chylomicrons are ultimately taken up by liverhepatocytesvia interaction betweenapolipoprotein Eand theLDL receptororlipoprotein receptor-related proteins.
In lipoproteins[edit]
Cholesterol is minimally soluble inwater;it cannot dissolve and travel in the water-based bloodstream. Instead, it is transported in the bloodstream bylipoproteinsthat are water-soluble and carry cholesterol andtriglyceridesinternally. Theapolipoproteinsforming the surface of the given lipoprotein particle determine from what cells cholesterol will be removed and to where it will be supplied.
The largest lipoproteins, which primarily transport fats from theintestinalmucosato theliver,are calledchylomicrons.They carry mostly fats in the form of triglycerides. In the liver, chylomicron particles release triglycerides and some cholesterol. The liver converts unburned food metabolites intovery low density lipoproteins(VLDL) and secretes them into plasma where they are converted to intermediate-density lipoproteins(IDL), which thereafter are converted tolow-density lipoprotein(LDL) particles and non-esterified fatty acids, which can affect other body cells. In healthy individuals, most of the LDL particles arelarge and buoyant(less dense, also known as lb-LDL) and they are cardiovascularly neutral: they have no negative and no positive effect on cardiovascular health. In contrast, large numbers ofsmall and denseLDL (sd-LDL) particles are strongly associated with the presence ofatheromatousdisease within the arteries. For this reason, total LDL is referred to as "bad cholesterol," although only a fraction of it is actually bad.
Standard chemistry panels typically include total triglyceride, LDL and HDL levels in the blood. Measuring the concentration of sd-LDL is expensive. However, since it is produced from VLDL, it can be inferred indirectly by estimating VLDL levels in the blood. That estimate is typically obtained by measuring triglyceride levels after at least eight hours of fasting, when chylomicrons have been totally removed from the blood by the liver. In the absence of chylomicrons, triglyceride levels have a much larger correlation with risk ofcardiovascular diseasesthan total LDL levels.
Intestine excretion[edit]
After being transported to the liver by HDL, cholesterol is delivered to the intestines via bile production. However, 92-97% is reabsorbed in the intestines and recycled viaenterohepatic circulation.
Cell uptake[edit]
Cholesterol circulates in the blood inlow-density lipoproteinsand these are taken into the cell byLDL receptor-mediatedendocytosisinclathrin-coated pits,and then hydrolysed in lysosomes.
Cell secretion[edit]
In response to low blood cholesterol, different cells of the body, mainly in theliverandintestines,start to synthesize cholesterol fromacetyl-CoAby the enzymeHMG-CoA reductase.This is then released into the blood.
Related medical conditions[edit]
Hyperlipidemia[edit]
Hyperlipidemia is the presence of elevated or abnormal levels oflipidsand/orlipoproteinsin theblood.
Lipid andlipoproteinabnormalities are extremely common in the general population, and are regarded as a highly modifiable risk factor forcardiovascular disease.In addition, some forms may predispose toacute pancreatitis.One of the most clinically relevant lipid substances ischolesterol,especially onatherosclerosisandcardiovascular disease.The presence of high levels of cholesterol in the blood is calledhypercholesterolemia.[6]
Hyperlipoproteinemiais elevated levels oflipoproteins.
Hypertriglyceridemia[edit]
Hypercholesterolemia[edit]
Hypercholesterolemia is the presence of high levels ofcholesterolin the blood.[6]It is not adiseasebut ametabolicderangement that can be secondary to many diseases and can contribute to many forms of disease, most notablycardiovascular disease.Familial hypercholesterolemiais a raregenetic disorderthat can occur in families, where sufferers cannot properly metabolise cholesterol.
Hypocholesterolemia[edit]
Abnormally low levels of cholesterol are calledhypocholesterolemia.
See also[edit]
References[edit]
- ^Molecular cell biology. Lodish, Harvey F. 5. ed.: - New York: W. H. Freeman and Co., 2003. Page 321. b ill.ISBN0-7167-4366-3
- ^"Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. The Expert Panel".Arch. Intern. Med.148(1): 36–69. 1988.doi:10.1001/archinte.148.1.36.PMID3422148.
- ^Ockene IS, Chiriboga DE, Stanek EJ, Harmatz MG, Nicolosi R, Saperia G, Well AD, Freedson P, Merriam PA, Reed G, Ma Y, Matthews CE, Hebert JR (2004). "Seasonal variation in serum cholesterol levels: treatment implications and possible mechanisms".Arch Intern Med.164(8): 863–70.doi:10.1001/archinte.164.8.863.PMID15111372.
- ^MacRury, SM; Muir, M; Hume, R (1992). "Seasonal and climatic variation in cholesterol and vitamin C: effect of vitamin C supplementation".Scottish Medical Journal.37(2): 49–52.doi:10.1177/003693309203700208.PMID1609267.S2CID22157704.
- ^Dobson, HM; Muir, MM; Hume, R (1984). "The effect of ascorbic acid on the seasonal variations in serum cholesterol levels".Scottish Medical Journal.29(3): 176–82.doi:10.1177/003693308402900308.PMID6533789.S2CID13178580.
- ^abDurrington P (2003). "Dyslipidaemia".Lancet.362(9385): 717–31.doi:10.1016/S0140-6736(03)14234-1.PMID12957096.S2CID208792416.
