Immune cells perform a previously unsuspected role in the brain that may contribute to obesity, according to a new study by UC San Francisco researchers. When the scientists fed mice a diet high in saturated milk fats, microglia, a type of immune cell, underwent a population explosion in the brain region called the hypothalamus, which is responsible for feeding behavior. The researchers used an experimental drug and, alternatively, a genetic approach to knock out these microglia, and both strategies resulted in a complete loss of microglia-driven inflammation in the hypothalamus. Remarkably, doing so also resulted in the mice eating less food each day than did their untreated counterparts, without any apparent ill effects. Furthermore, removing microglia from mice only reduced food intake when the content of saturated fat from milk in their diets was high. It had no effect on mice fed a low-fat diet, or a diet high in other types of fat, including olive oil or coconut oil. UCSF postdoctoral fellow Martin Valdearcos Contreras, Ph.D., first author on the paper, published online on December 11, 2014 in an open-access article in Cell Reports, discovered that when mice consumed large amounts of saturated fats, the fat entered their brains and accumulated in the hypothalamus. According to the senior scientist for the study, Suneil Koliwad, M.D., Ph.D., an assistant professor of medicine at the UCSF Diabetes Center, the microglia senses the saturated fat and sends instructions to brain circuits in the hypothalamus. These instructions are important drivers of food intake, he said. Microglia are primarily known for causing inflammation in the brain in response to infection or injury, but the new study indicates that they also play a key role in shaping the brain's response to diet, according to Dr. Koliwad.
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