Step 1 - Biochem 5
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2012-08-12 06:29
cholesterol synthesis
| Question | Answer |
|---|---|
| Cholesterol synthesis | -Rate-limiting step is catalyzed by HMG-CoA reductase (converts HMG-CoA to mevalonate) - 2/3 of plasma cholesterol is esterified by lecithin-cholesterol acyltransferase (LCAT) - Statins inhibit HMG-CoA reductase |
| Essential fatty acids | Linoleic and linolenic acids - Arachidonic acid, if linolenic is absent - Eiconasoids are dependent on essential fatty acids. |
| Pancreatic lipase | degradation of dietary TG in small intestine |
| Lipoprotein lipase (LPL) | degradation of TG circulating in chylomicrons and VLDLs |
| Hepatic TG lipase (HL) | degradation of TG remaining in IDL. |
| Hormone-sensitive lipase | degradation of TG stored in adipocytes. |
| Lecithin-cholesterol acyl transferase (LCAT) | -Catalyzes esterification of cholesterol. -Nascent HDL becomes mature HDL |
| Cholesterol ester transfer protein (CETP) | mediates transfer of cholesterol esters to other lipoprotein particles |
| Apolipoprotein A-I | Activates LCAT. |
| Apolipoprotein B100 | Binds to LDL receptor, mediates VLDL secretion. |
| Apolipoprotein C-II | Cofactor for LPL. |
| Apolipoprotein B-48 | Mediates chylomicron secretion. |
| Apolipoprotein E | Mediates Extra (remnant) uptake |
| Lipoproteins | Composed of varying proportions of cholesterol, triglycerides(TGs) and phospholipids. LDL and HDL carry most cholesterol. |
| Chylomicron function/route | -Delivers dietary TGs to peripheral tissue. -Delivers cholesterol to liver in the form of chylomicron remnants, which are mostly depleted of their TAGS - Secreted by intestinal epithelial cells. |
| Apolipoproteins in chylomicron | B-48, A, C, E |
| VLDL function/route | Delivers hepatic TGs to peripheral tissue, secreted by liver |
| Apolipoproteins in VLDL | B-100, C, E |
| IDL function/route | Formed in the degradation of VLDL. Delivers cholesterol to liver, where they are degraded to LDL |
| Apolipoproteins in IDL | B-100 and E |
| LDL function/route | -Delivers hepatic cholesterol to peripheral tissues. -Formed by LPL modification of VLDL in the peripheral tissue. -Taken up by target cells via receptor-mediated endocytosis. |
| Apolipoprotein in LDL | B-100 |
| HDL function/route | -Mediates reverse cholesterol transport from periphery to liver. -Acts as a repository for apoC and apoE (which are needed for chylomicron and VLDL metabolism). - Secreted from both liver and intestine (Looks lik e liver prefers CE over CH) |
| Familial dyslipidemias I - hyperchylomicronemia | 1. Increased chylomicron 2. Elevated TG, cholesterol 3. LPL deficiency or altered apoliprotein C, causes pancreatitis, hepatosplenomegaly and eruptive/pruritic xanthomas (no increase in risk for atherosclerosis) |
| Familial dyslipidemias IIa - familial hypercholesterolemia | 1. Increased LDL 2. Elevated blood cholesterol 3. Autosomal dominant - absent or ↓ LDL receptors. -Causes accelerated atherosclerosis, tendon (Achilles) xanthomas and corneal arcus~ (2 tendons, 2 eyes) |
| Familial dyslipidemia IV - hypertriglyceridemia | 1. Increased VLDL 2. Elevated Triglyceride in blood 3. Hepatic overproduction of VLDL - causes pancreatitis |
| Abeta-lipoproteinemia | -Hereditary inability to synthesize lipoproteins due to deficiencies in apoB100 and apo b48 -autosomal recessive, - Sx appear in the first few months of life. -Intestinal biopsy shows accumulation within enterocytes due to inability to export absorbed lipid as chylomicrons. . Findings: failure to thrive, steatorrhea, acanthocytosis(spikey RBC), ataxia, night blindness |
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