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AJP - Regulatory, Integrative and Comparative Physiology, Vol 263, Issue 6 1228-R1234, Copyright © 1992 by American Physiological Society
ARTICLES |
A. Takahashi, M. Sudo, Y. Minokoshi and T. Shimazu
Department of Neuropsychopharmacology, Gunma University School of Medicine, Tsumura, Japan.
Electrical stimulation of the ventromedial hypothalamus (VMH) increased the rate constant of glucose uptake in rat heart and brown adipose tissue (BAT), as measured in vivo by the 2-deoxy-D-[3H]glucose method. The increase in glucose uptake in BAT was abolished by local sympathetic denervation. To analyze the mechanism of this hypothalamic modulation, the effects of VMH stimulation and insulin treatment on the number and dissociation constant (Kd) of glucose transporters in the plasma and microsomal membranes were examined by means of [3H]cytochalasin B binding. VMH stimulation did not alter either the number or Kd value of glucose transporters in plasma and microsomal membranes prepared from heart and BAT, whereas insulin treatment increased the number of glucose transporters in the plasma membranes and decreased those in the microsomal membranes. D-Glucose transport activity was also measured with the same plasma membrane vesicles. An apparent functional activity of transporters was detected to be increased in the heart and BAT plasma membranes after VMH stimulation but not after insulin treatment. These results suggest that VMH stimulation enhances glucose utilization in heart and BAT via sympathetic innervation and that the mechanism by which VMH stimulation increases tissue glucose uptake is different from that of insulin, possibly causing an activation of glucose transporters present in the plasma membrane.
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