News Release

Hungry? A newly discovered neural circuit may be the cause

Peer-Reviewed Publication

American Association for the Advancement of Science (AAAS)

A particular subset of neurons located in an enigmatic region of the hypothalamus plays a central role in regulating feeding and body weight in mice, a new study reveals. The results illuminate a previously unknown neural mechanism of feeding regulation and offer new perspectives on understanding changes in appetite. Knowledge of the function of a region of the hypothalamus called the nucleus tuberalis lateralis, or NTL, is scarce, though scientists seek to better understand it as damage to this brain region in patients results in marked declines in appetite, and in rapid loss in body weight. To further explore any role the NTL may have in regulation of feeding and body weight, Sarah Xinwei Luo and colleagues observed the behavior of somatostatin (SST) neurons in the NTL using a mouse model. The authors found that the SST neurons were activated by both hunger (following overnight food deprivation) and after administration of the hunger hormone, ghrelin. Selective activation and deactivation of the neurons, using both drugs and optogenetics, demonstrated that eating behavior could be controlled - activation increased eating behavior, while inhibition significantly reduced it. Total elimination of the neurons altogether resulted in decreased daily food intake as well as gradual weight gain. According to the study's findings, SST neurons are required for controlling healthy eating and body weight. In a related Perspective, Sabrina Diano notes that Luo et al.'s results are highly relevant - efforts to affect body weight and other physiological impairments associated with aberrant feeding behaviors, like obesity or anorexia nervosa, have been futile. Despite the translational uncertainty between the neural circuitry of mice and humans, Luo et al.'s results are novel and warrant further investigation, says Diano.


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