Buffet belly

Farley, Suzanne

doi:10.1038/nrn1170

Research Highlight
Published: July 2003

Buffet belly

Suzanne Farley

Nature Reviews Neuroscience volume 4, page 521 (2003)Cite this article

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In a study published in Nature Medicine, Obici et al. selectively reduced lipid oxidation in the hypothalamus by decreasing the activity of CPT1, an enzyme that regulates the entry of long-chain fatty acids (LCFAs) into mitochondria. The authors used intracerebroventricular infusion of a CPT1-specific ribozyme or pharmacological inhibitors to reduce CPT1 activity — and consequently increase the hypothalamic concentration of LCFAs — in the arcuate nuclei of rats. The result was a 50% reduction in voluntary food intake, an effect that lasted at least 48 hours after a single dose of ribozyme or inhibitor.

To assess the impact of CPT1 inhibition on glucose homeostasis, the rate of glucose infusion required to prevent hypoglycaemia in CPT1-inhibited rats was measured while maintaining the peripheral insulin concentration at a fixed basal level. Inhibition of CPT1 necessitated a rate of glucose administration that was up to fivefold greater than in untreated controls. The authors showed that suppression of endogenous glucose production — not stimulation of glucose uptake — accounted for this excessive requirement for exogenous glucose.

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ORIGINAL RESEARCH PAPER

Obici, S. et al. Inhibition of hypothalamic carnitine palmitoyltransferase-1 decreases food intake and glucose production. Nature Med. 9, 756–761 (2003)
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