Insulin receptor function and insulin effects on glucose metabolism in adipocytes from ventromedial hypothalamus-lesioned rats.
To investigate the mechanism of the development of insulin resistance in hypothalamic obesity, we studied insulin binding, glucose transport, and glucose oxidation in adipocytes from ventromedial hypothalamus (VMH)-lesioned rats 1 and 2 weeks after injury. One week after injury, insulin binding and insulin-stimulated glucose oxidation were increased, but insulin-stimulated glucose transport was similar to control. Two weeks after injury, insulin binding and insulin-stimulated glucose transport were similar to control, but insulin-stimulated glucose oxidation was decreased. Thus, cellular insulin responsiveness was increased in adipocytes from VMH-lesioned rats 1 week after injury; this increase in insulin responsiveness was due mainly to the increased intracellular glucose metabolism. On the other hand, cellular insulin resistance existed in adipocytes from VMH-lesioned rats 2 weeks after injury; this insulin resistance was also due mainly to a defect in intracellular glucose metabolism.
D000273:Adipose Tissue / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D000818:Animals; D003847:Deoxyglucose / Q000378:metabolism; D005947:Glucose / Q000378:metabolism*; D007031:Hypothalamus / Q000502:physiology*; D007033:Hypothalamus, Middle / Q000502:physiology*; D007328:Insulin / Q000378:metabolism / Q000494:pharmacology*; D008297:Male; D010084:Oxidation-Reduction; D051381:Rats; D011972:Receptor, Insulin / Q000378:metabolism*
D007328:Insulin; D003847:Deoxyglucose; D011972:Receptor, Insulin; D005947:Glucose