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& u metabolism of HDL in type 2 DM is complicated by the common presence of obesity and insulin resistance-associated dyslipidemia in this group. An inverse relationship between plasma insulin (or C-peptide), measures of insulin resistance, and HDL cholesterol levels has been identified consistently. Fractional catabolism of apo A-I is increased in type 2 DM with low HDL, but that is no different from what is seen in nondiabetics with similar lipoprotein profiles. While Apo A-I levels are reduced consistently, correction of hypertriglyceridemia does not usually alter apo A-I levels.

In summary, HDL levels are normal or even elevated in tightly controlled, well-insulinized patients with type 1 DM, whereas low HDL cholesterol concentrations are a hallmark of type 2 DM. The latter abnormality has several defined components, including increased fractional removal of apo A-I from plasma and increased CETP-mediated transfer of HDL cholesteryl esters to apo B lipoproteins. Defective apo A-I lipoprotein-mediated efflux of cellular free cholesterol (possibly related to defects in ABC1), defective LCAT activity, increased selective delivery of HDL2 cholesteryl ester to hepatocytes via SRB1 (although this might be antiatherogenic), and possible effects of glycosylation of HDL apo C-II, apo C-III, and apo E are other potential key players (Table 4).

Table 4 Abnormalities in Fasting Lipid Metabolism

Type of diabetes

Poorly controlled

Well controlled

Type 1

Increased VLDL secretion

Normal or low VLDL secretion

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