Prior to summarizing the influence of IR on lipid metabolism, it is instructive to briefly review some of the functions insulin plays in its role as the "master metabolic hormone." Insulin has a number of actions beyond the promotion of cellular uptake of glucose. It suppresses hepatic gluconeogenesis and shifts the metabolic state of tissues (particularly skeletal muscle) toward the oxidation and storage (as glycogen) of energy from carbohydrate. At the same time, insulin suppresses the activity of hormone-sensitive lipase. This, in turn, reduces the release of free fatty acids (FFAs) from adipose tissues into the circulation and thereby lowers the availability of FFAs as a substrate for oxidation. Insulin also stimulates lipoprotein and hepatic lipases, enhancing the hydrolysis of TGs in circulating lipoproteins and allowing their FFAs to move into cells. In the liver, insulin stimulates the breakdown of apolipoprotein (Apo) B.
Not all of the actions of insulin may be impaired to the same degree. Some of the metabolic abnormalities associated with IR may result from insufficient insulin action.
In patients with IR who do not have diabetes, normal glucose levels are maintained through excessive insulin secretion (compensatory hyperinsulinemia). Thus, some of metabolic abnormalities associated with IR may not result from impaired insulin action, but rather from overstimulation of insulin-mediated processes that are not impaired.
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