Abstract

The levels of insulin, free fatty acids (FFA), and triglycerides in rat sera increase with age. The increase in serum FFA levels accompanied the stimulation of basal lipolysis (i.e., lipolysis in the absence of lipolytic agents) in fat cells and enlargement of the diameter of the cells. An overnight fast resulted in a significant increase in basal lipolysis in fat cells from 6- and 8-week-old rats. Although insulin inhibited lipolysis induced by norepinephrine and ACTH at a concentration of 10(-10) M, it failed to inhibit basal lipolysis even at a concentration of 10(-6) M. Propranolol, another antilipolytic agent like insulin, also did not affect basal lipolysis. Insulin did not inhibit the accelerated basal lipolysis in enlarged fat cells, fasted fat cells, and sonicated cells. These results indicate that insulin inhibits only the lipolysis induced by lipolytic agents such as norepinephrine and ACTH but not the basal lipolysis found in the absence of lipolytic agents. The possibility that free fatty acids produced by enlarged fat cells initiate insulin resistance and diabetes mellitus, is discussed.

Highlights

  • The levels of insulin, free fatty acids (FFA), and triglycerides in rat sera increase with age

  • It seems likely that the rise in serum FFA levels is due to stimulation of basal lipolysis in fat cells

  • Insulin inhibited lipolysis induced by norepinephrine or adrenocorticotropic hormone (ACTH) in fat cells, it did not affect basal lipolysis in these cells (Figs. 2 and 4)

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Summary

Introduction

The levels of insulin, free fatty acids (FFA), and triglycerides in rat sera increase with age. Plasma FFA levels are affected by fat cell lipolysis which is regulated by hormone-dependent and hormone-independent lipolytic activities. Our previous study demonstrated that basal lipolysis is elevated in the enlarged fat cells of obese rats as a result of a reduction in the surface phosphatidylcholine concentration of endogenous lipid droplets [1, 2]. An active hormone-sensitive lipase (HSL) is present in fat cells even in the absence of lipolytic hormones, and phosphatidylcholine on the surface of endogenous lipid droplets causes inhibition of the lipolytic action of HSL. The present investigation was designed to clarify whether insulin inhibits basal lipolysis in rat fat cells

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