Eating Less

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Science  13 Apr 2001:
Vol. 292, Issue 5515, pp. 171-173
DOI: 10.1126/science.292.5515.171f

Body weight in mammals is regulated by a neuroendocrine feedback loop. Fat tissue itself serves as an endocrine end-organ, secreting leptin, which acts in the hypothalamus of the brain and results in the stimulation of melanocortin receptors and inhibition of food intake, which in turn lowers the amount of body fat. Obesity can be caused by dysregulation at several points in this system: for instance, via loss-of-function mutations in the leptin gene or receptor and similar mutations in melanocortin genes or their receptors. But how might this system cause too little food intake, as in the disorder anorexia nervosa?

Vink et al. posit that decreased activity in an endogenous melanocortin antagonist—agouti-related protein—could contribute to such starvation syndromes. They examine the gene for agouti-related protein in 145 patients with anorexia nervosa and 244 controls, and identify two polymorphisms that occur together and are found in a significantly greater percentage of the patients than in the controls. The presence of this haplotype confers a relative risk of 2.63 on its carriers and so does not apply to all cases of anorexia nervosa. Nevertheless, identification of a gene that, when dysfunctional, would decrease food intake presents a potential therapeutic target for treating eating disorders. — KK

Mol. Psych.6, 325 (2001).

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