Defective cerebral glucose utilization in diet-induced obese rats.
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.
Levin
B E
BE
Department of Veterans Affairs Medical Center, East Orange 07019.
D000818:Animals; D001345:Autoradiography; D001921:Brain / Q000378:metabolism*; D003847:Deoxyglucose / Q000493:pharmacokinetics; D004032:Diet; D004198:Disease Susceptibility; D005947:Glucose / Q000378:metabolism*; D008297:Male; D009765:Obesity / Q000209:etiology* / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D012439:Saccharin / Q000008:administration & dosage / Q000494:pharmacology; D014018:Tissue Distribution
D003847:Deoxyglucose; D012439:Saccharin; D005947:Glucose