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Pathophysiology of Hyperlipidemia

Pathophysiology of Hyperlipidemia 

An understanding of the biology of the lipoproteins and the pathophysiology of hyperlipidemic states is essential to the rational choice of treatment regimen.
• Exogenous pathway:
Route of uptake of dietary lipids: Chylomicrons (CM) are complexes of triglycerides (TG), cholesteryl esters (CE), and apoproteins. After the removal of triglycerides they become chylomicron remnants .
Chylomicrons are degraded by lipoprotein lipase on endothelial cells of adipose tissue and muscle. After removal of TG for storage, the CM remnants are transported to the liver. This results in dietary TG stored in adipose tissue and muscles.

• Endogenous pathway:
Route for distribution of cholesteryl esters (CE) from liver to target cells :VLDL is secreted by the liver into plasma and transported to adipose
tissue and muscles, where lipoprotein lipase extracts most triglycerides. The remnant IDL is either taken up by the liver or circulated until the remaining triglycerides are removed forming LDL particles, rich in cholesterol. LDL is cleared from plasma through LDL receptor-mediated endocytosis. This results in transfer of TG from liver to target cells via VLDL, as well as, transfer of CE from liver to target cells via LDL.
Reverse cholesterol transport is a pathway where cholesterol is transported from atherosclerotic plaques or other lipids back to liver to be
excreted into the faecus via bile. As cell dies and the cell membranes turnover, free cholesterol is released into the plasma. It is immediately absorbed into HDL particles, esterified with a long chain fatty acid by lecithin cholesterol acyl transferase (LCAT), and transferred to VLDL or IDL by a cholesteryl
ester transfer protein in plasma. Eventually, it is taken up by the liver as IDL or LDL, thus resulting in the recovery of cholesterol from cell membranes and reincorporation into LDL pool or return to liver. 

  • Route for cholesterol recovery

Reverse cholesterol transport is a pathway where cholesterol is transported from atherosclerotic plaques or other lipids back to liver to be excreted into the faecus via bile. As cell dies and the cell membranes turnover, free cholesterol is released into the plasma. It is immediately absorbed into HDL particles, esterified with a long chain fatty acid by lecithin cholesterol acyl transferase (LCAT), and transferred to VLDL or IDL by a cholesteryl ester transfer protein in plasma. Eventually, it is taken up by the liver as IDL or LDL, thus resulting in the recovery of cholesterol from cell membranes and reincorporation into LDL pool or return to liver.Liver synthesizes 2/3rd of the total cholesterol made in the body. The rate limiting enzyme is 3-hydroxy-3-methylglutaryl(HMG)-CoA reductase and provides feedback regulation by controlling the cholesterol concentrations in cells.

  • De novo cholesterol biosynthesis

Bile salts are synthesized from cholesterol in the liver, released into the intestine, and recycled. A small amount of bile acid is excreted. This results in 
conversion of liver cholesterol to bile salts for excretion.

  • Cholesterol excretion by enterohepatic circulation

Bile salts are synthesized from cholesterol in the liver, released into the intestine, and recycled. A small amount of bile acid is excreted. This results in 
conversion of liver cholesterol to bile salts for excretion.


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