Pathogenesis of Atherogenic Dyslipidemia

Whole-Body Obesity

In the presence of whole-body obesity, plasma NEFA levels usually are elevated.^[57] This is because adipose tissue retains a basal secretion of NEFA that cannot be completely suppressed by elevated insulin concentrations. Obesity per se does not cause insulin resistance in adipose tissue; in many overweight persons, an elevated plasma insulin can still normally suppress NEFA release.^[58] Nonetheless, the sheer bulk of excess adipose tissue leads to a chronically high level of NEFA. This is particularly so in the fasting state. Therefore, obesity per se can cause insulin resistance in skeletal muscle and hepatic lipid overload even in the absence of insulin resistance in adipose tissue.

On the other hand, not all overweight persons manifest atherogenic dyslipidemia and the insulin resistance syndrome. This is partly because they are able to maintain enough insulin sensitivity in adipose tissue to prevent continued elevations of plasma NEFA. Variability of degrees of insulin resistance of different forms of adipose tissue have become a subject of great interest; specifically, adipose tissue in the trunk (upper body obesity) appears to be insulin resistant. This is further discussed elsewhere in this supplement (see Pi-Sunyer, p. 28).

© 2000 Cliggott Publishing, Division of CMP Healthcare Media

Cite this: Pathogenesis of Atherogenic Dyslipidemia - Medscape - May 01, 2000.