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Hap1 protein links circulating insulin to brain circuits that regulate feeding behavior in mice

evel and activity of GABA receptors in the hypothalamus.

"We concluded that increased levels of Hap1 correlated with increased feeding behavior in the mice, and our research helps explain how Hap1 is linked to feeding-related molecules such as insulin, and to hypothalamic neuronal function," said Xiao-Jiang Li, PhD, professor of human genetics at Emory University School of Medicine and senior author of the study. "GABA is known to have a stimulating effect on feeding behavior. Because insulin decreases Hap1 levels, and reducing Hap1 decreases the GABA receptor activity, we believe Hap1 is the link between circulating insulin and the regulation of GABA receptors in the hypothalamus in controlling eating behavior."

"Scientists know that diabetes and obesity are related to abnormalities of hypothalamic function," Li said. "This is a complicated pathway, and Hap1 can help us explain it and hopefully manipulate it to treat disorders associated with abnormal energy balance in the brain."

Stuart A. Lipton, MD, PhD, director and professor of the Center for Neuroscience and Aging at the Burnham Institute for Medical Research in La Jolla, further stated, Òthe new work opens up additional targets for obesity research. For example, a drug that decreases Hap1 in the hypothalamus would decrease the electrical drive that underlies eating behavior, resulting in weight loss and potentially longer lifespan.Ó


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Source:Emory University Health Sciences Center


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