Abstract
The paradigm of obesity leading to insulin resistance and type 2 diabetes is examined in relation to dyslipidemia, which typically consists of high levels of triglycerides (TG) and low levels of high-density lipoprotein (HDL). Kinetic studies with stable isotope-labeled amino acid precursors have shown that the development of visceral obesity, as well as type 2 diabetes, leads to overproduction of the apolipoprotein B-100 and TG in very low-density lipoproteins. Elevated plasma levels or increased flux of albumin-bound free fatty acids to the liver appear to be underlying metabolic events in this process. Low levels of HDL are due to increased catabolism, which can be related to TG enrichment.
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