Abstract

Insulin resistant states are characterized by receptor and post-receptor defects in insulin action. When the insulin resistant state progresses, elevated levels of insulin are accompanied by increasing levels of glucose. In a previous paper we demonstrated that treatment of isolated adipocytes with high levels of insulin led to a decrease in insulin binding as well as a decrease in basal and insulin-stimulated lipid synthesis. The results of the present study establish that the addition of high concentrations of glucose in combination with a level of insulin, does not modify the decrease in binding of insulin to its receptor. However, the decrease in lipid synthesis previously observed in the presence of high concentrations of insulin was completely overcome by the presence of high glucose.

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