The hypothalamus has been implicated in the development of obesity in both humans1 and experimental animals2. The syndrome of hypothalamic obesity results from destruction of the ventromedial region of the hypothalamus3, and investigations of the influences of the hypothalamus on lipid metabolism have been directed chiefly at understanding the mechanism underlying obesity2,4,5. There have been few studies of the effects on lipolysis and lipogenesis in adipose tissue after stimulation of the ventromedial and lateral hypothalamic (LH) nuclei, which may act reciprocally in regulating certain types of peripheral metabolism6–9. We have shown10 that electrical stimulation of the ventromedial hypothalamic nucleus (VMH) causes lipolysis in adipose tissue, detected by a rapid rise in the plasma glycerol concentration, whereas electrical stimulation of the LH has no such effect. It is not known whether hypothalamic stimulation of either the VMH or the LH affects lipogenesis in adipose tissue. We have investigated this problem by measuring the incorporation of tritium from 3H2O into fatty acids in vivo. This is the most reliable method for measuring the rate of fatty acid biosynthesis, because it is independent of the carbon precursor11,12. Surprisingly, electrical stimulation of the VMH enhanced fatty acid synthesis in brown adipose tissue, but not in white adipose tissue or the liver, without the intervention of insulin secretion. Electrical stimulation of the LH, however, had no appreciable effect on lipid synthesis in either type of adipose tissue.
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European Journal of Applied Physiology and Occupational Physiology (1986)