Effects of FFAs on Hepatic VLDL Production

Lipoprotein metabolism in insulin resistance and type 2 diabetes will be covered elsewhere in this book and has been reviewed in more detail elsewhere (82). Briefly, the hypertriglyceridemia of insulin resistance and type

2 diabetes is primarily owing to VLDL overproduction, with reduced VLDL clearance playing a role in some instances. Increased FFA flux from adipose tissue acts as a driving force to increase secretion of VLDL, which is regulated by lipid substrate availability. VLDL overproduction in insulin resistance and type 2 diabetes occurs as a result of a composite set of factors over and above the increased flux of fatty acids from extrahepatic tissues to the liver, including increased hepatic de novo fatty acid synthesis, preferential esterification versus oxidation of fatty acids, reduced posttranslational degradation of apo B, and overexpression of MTP, the latter being an important chaperone for the assembly of apoB-containing lipoproteins in the liver and intestine (82). Low HDL-cholesterol and small, dense, more atherogenic LDL are other prominent features of the insulin resistance-associated dyslipidemia, and occur in part secondary to particle compositional changes that occur in hypertriglyceridemic states (177).

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