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Research Article Free access | 10.1172/JCI108984
Department of Medicine, University of California, Torrance, California 90509
Los Angeles School of Medicine, Harbor General Hospital Campus, Torrance, California 90509
Find articles by Nishizawa, Y. in: JCI | PubMed | Google Scholar
Department of Medicine, University of California, Torrance, California 90509
Los Angeles School of Medicine, Harbor General Hospital Campus, Torrance, California 90509
Find articles by Bray, G. in: JCI | PubMed | Google Scholar
Published March 1, 1978 - More info
We have explored the effects of ventromedial hypothalamic lesions on the mobilization of free fatty acids in rats exposed to several stresses. The rise in free fatty acids and glycerol in response to norepinephrine had the same time-course and dose-response characteristics in the sham-operated and lesioned animals, indicating comparable degrees of peripheral responsiveness to this hormone. Forced swimming significantly lowered insulin and increased glycerol and free fatty acids more in control than in ventromedial hypothalamic-lesioned rats. During fasting, the rise in glycerol and free fatty acids was smaller in the lesioned rats, but the fall in insulin was greater. Exposure to cold raised fatty acids and glycerol more in the control than in the sham-operated animals, but had no significant effect on plasma insulin or glucose concentration. Injection of 2-deoxyglucose was done on lesioned or control rats with intact or removed adrenal medullas. The rise in free fatty acids and glycerol was less in the lesioned rats than in the controls, and was not affected by adrenodemedullation. The rise in glucose, however, was completely blocked in the adrenodemedullated rats. Changes in insulin were small and not statistically significant. The reduced mobilization of fatty acids from adipose tissue depots after ventromedial hypothalamic injury is consistent with the hypothesis that the ventromedial hypothalamic region serves to modulate activation of the sympathetic nervous system.