Increase of postheparin plasma-lipoprotein-lipase activity in ventromedial-hypothalamic obesity in rats

Postheparin plasma-lipoprotein lipase (LPL) and hepatic triglyceride lipase (H-TGL) were investigated in rats 1 week after ventromedial-hypothalamic lesions. The enzyme activities were measured using radio-labelled triolein as a substrate. Two lipases were measured separately using specific antiserum prepared against H-TGL. VMH-lesioned rats fed ad lib. showed an increase in plasma LPL with normal H-TGL activity and an elevation of plasma insulin. There was a positive correlation between plasma-LPL activity and insulin levels in VMH-lesioned rats. When rats were examined after overnight fast, VMH-lesioned rats again showed an increase in plasma LPL with normal H-TGL activity and an elevation of plasma insulin. There was also a positive correlation between plasma LPL activity and insulin levels. In order to examine the effect of insulin, rats were treated with daily doses of 3 units of insulin for 1 week. Rats fed ad lib. were insulin treatment showed an increase in plasma LPL with normal H-TGL activity. These results indicate that hyperinsulinemia which was produced by VMH lesions may increase postheparin plasma-LPL activity. We speculate that this increase in plasma-LPL activity mainly reflects that of adipose tissue. The increase of LPL activity can accelerate fat deposition into adipose tissue, contributing to one of the factors causing hypothalamic obesity.