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Figure 1 Mechanisms of the Production of the "Dyslipidemic Triad"
An increased flux of free fatty acids (FFA) from adipose tissue can result from insulin resistance or a defect in the acylation stimulatory protein (ASP) pathway. Enhanced hepatic uptake of FFA leads to increased triglyceride (TG), apolipoprotein (apo) B, and very-low-density lipoprotein (VLDL) production. The TG in VLDL is exchanged for cholesteryl esters (CE) from low-density lipoproteins (LDL) and high-density lipoproteins (HDL) by the cholesteryl ester transport protein (CETP), producing CE-depleted LDL and HDL. The TG in the core of LDL and HDL is then hydrolyzed by lipases, producing both small, dense LDL and HDL. Such HDL is more likely to be excreted by the kidney, resulting in low HDL-C levels. HL = hepatic lipase; IDL = intermediate-density lipoprotein; IR = insulin resistance; LCAT = lecithin-cholesterol acyltransferase; LPL = lipoprotein lipase.
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