Genetic switch regulating satiety and body weight identified

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Science Daily.

Why do we get fat and why is it so difficult for so many people to keep off excess weight? Researchers in the Reseach Unit Neurobiology of Diabetes led by Dr. Paul Pfluger and at the Institute for Diabetes and Obesity led by Prof. Dr. Matthias Tschöp have now identified a new component in the complex fine-tuning of body weight and food intake. They found that the enzyme histone deacetylase 5 (HDAC5) has a significant influence on the effect of the hormone leptin. This hormone plays a crucial role in triggering satiety and thus on how the body adapts to a changing food environment.

Pfluger describes the results as follows: “HDAC5 is an important link in the communication between our fat tissue and hunger centers in the brain.” Initial experiments have shown that the production and activity of HDAC5 in our control center for energy balance, the hypothalamus, is increased by a high-fat diet, by enlarged fat deposits and by the satiety hormone leptin. Dhiraj Kabra, first author of the study, added: “HDAC5 is a molecular switch in the brain that helps the body to recognize how full the fat depots are. Without HDAC5, we cannot adapt our food intake or curb our fat deposition.”

Disruption of the signaling pathway leads to obesity

According to the scientists, mice unable to produce HDAC5 respond significantly worse to leptin — a condition referred to as leptin resistance.

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