AJP - Regulatory, Integrative and Comparative Physiology, Vol 265, Issue 4 786-R791, Copyright © 1993 by American Physiological Society
Determinants of fasting hypertriglyceridemia in ventromedial hypothalamic obesity in rats
S. Inoue, S. Satoh, K. Tanaka, Y. Takamura and T. Murase
Third Department of Internal Medicine, Yokohama City University, Japan.
The present study investigated the mechanism of fasting
hypertriglyceridemia in ventromedial hypothalamic (VMH) obesity by
measurement of post-heparin plasma lipoprotein lipase (LPL) activity,
triglyceride secretion rate (TGSR), and plasma insulin. One week after VMH
lesions, when the lesioned rats were gaining weight rapidly (the dynamic
phase), they showed normal plasma triglyceride levels with increased plasma
LPL activity and TGSR. There was a positive correlation between
hyperinsulinemia and elevated plasma LPL activity or TGSR in VMH-lesioned
rats, while no correlation was observed in control rats. Ten weeks after
VMH lesions, when the rats had become obese and reached a steady-state
weight gain (the static phase), they showed hypertriglyceridemia with
increased plasma LPL activity and TGSR. There was, again, a positive
correlation between hyperinsulinemia and elevated plasma LPL activity or
TGSR in VMH-lesioned rats. These results suggest a possible mechanism of
fasting hypertriglyceridemia in these rats; in the dynamic phase adipose
tissue adequately takes up circulating triglyceride because the tissue has
sufficient take-up capacity and hence hypertriglyceridemia does not
develop. In the static phase the tissue cannot adequately take up
circulating triglyceride because of a limitation of its capacity, resulting
in hypertriglycemia despite enhanced triglyceride secretion and increased
LPL activity in both phases.
