AJP - Regulatory, Integrative and Comparative Physiology, Vol 261, Issue 4 787-R792, Copyright © 1991 by American Physiological Society

ARTICLES

Defective cerebral glucose utilization in diet-induced obese rats

B. E. Levin
Department of Veterans Affairs Medical Center, East Orange 07019.

A neural mechanism may underlie the divergent weight gain patterns of rats fed a high-energy diet; half develop diet-induced obesity (DIO), whereas the rest are diet resistant (DR). Male rats were fed chow (n = 14) or a high-energy diet for 3 mo with the development of DIO (n = 11) or DR (n = 12). DIO rats had 159-219% heavier retroperitoneal fat pads and 158% higher plasma insulin levels than chow-fed and DR rats, but plasma glucose levels were equal. Rats were trained to drink glucose after an overnight fast and were tested for local cerebral glucose utilization using 2-deoxy-D-[14C]glucose autoradiography in the presence or absence of 0.15% saccharin substituted for glucose. Saccharin intake increased 2-deoxyglucose uptake in the rostral nucleus tractus solitarius of DR but not DIO or chow-fed rats. Also, DIO rats had reduced basal 2-deoxyglucose uptake in the central amygdaloid nucleus. High-energy diet intake was associated with saccharin-induced depression of 2-deoxyglucose uptake in the inferior olive and increased utilization in the medial amygdaloid nucleus of both DR and DIO rats. Thus DIO rats have diminished basal and food-related neuronal activity in certain brain areas involved in food intake and autonomic function. Furthermore, dietary content affects glucose utilization in areas not usually associated with these functions.

This article has been cited by other articles:

				B. E. Levin Arcuate NPY neurons and energy homeostasis in diet-induced obese and resistant rats Am J Physiol Regulatory Integrative Comp Physiol, February 1, 1999; 276(2): R382 - R387. [Abstract] [Full Text] [PDF]