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From: Chapter 166. Disorders of Lipid and Lipoprotein Metabolism
Rudolph's Pediatrics, 22e, 2011
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Pathophysiology of the dyslipidemic triad. The dyslipidemic triad is often present in familial combined hyperlipidemia (FCHL), hyperapoB, and metabolic syndrome. In the dyslipidemic triad (high VLDL-TG, increased numbers of small dense LDL-P, and decreased HDL-C), increased flux of free fatty acids (FFA) from adipose tissue, often due to insulin resistance or defects in the action of the acylation stimulatory protein (ASP), enhances hepatic uptake of FFA, leading to increased production of TG, apoB, and VLDL. The increased secretion of VLDL-TG promotes a greater exchange of TG (triglyceride) in VLDL for cholesteryl esters (CE) in LDL and HDL by cholesterol ester transfer protein (CETP). This results in CE-depleted but TG-enriched LDL and HDL. When TG in LDL and HDL is hydrolyzed by hepatic lipase (HL), smaller, denser LDL and HDL are produced. Such HDL is more likely to be excreted by the kidneys, resulting in low HDL-C levels.
Date of download: 9/18/2016
Copyright © 2016 McGraw-Hill Education. All rights reserved.