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Review
. 2000 Aug;106(4):453-8.
doi: 10.1172/JCI10762.

Insulin resistance and cardiovascular disease

H N Ginsberg  1
Affiliations
Review

Insulin resistance and cardiovascular disease

H N Ginsberg. J Clin Invest. 2000 Aug.
No abstract available

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Figures

Figure 1
Figure 1
A simplified model relating insulin resistance to dyslipidemia and cardiovascular disease. Insulin resistance at the adipocyte results in increased release of fatty acids into the circulation. A similar accumulation of fatty acids could arise from defects in fatty acid transporters or intracellular binding proteins. Increased FFA flux to the liver stimulates the assembly and secretion of VLDL resulting in hypertriglyceridemia. In addition, VLDL stimulates the exchange of cholesteryl esters from both HDL and LDL for VLDL TG. ApoA-I can dissociate from TG-enriched HDL. This free apoA-I is cleared rapidly from plasma, in part by excretion through the kidney, thus reducing the availability of HDL for reverse cholesterol transport. TG-enriched LDL can undergo lipolysis and become smaller and more dense. Low levels of HDL and the presence of small dense LDL are each independent risk factors for cardiovascular disease. IR, insulin resistance; CE, cholesteryl ester; SD, small dense.
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