Molecule links brain to blood sugar level

When we eat a meal, the body’s typical reaction is a rise in blood glucose levels, decreased appetite, production of insulin by the pancreas, and storage of excess sugar in the liver. Yale researchers have now identified a key molecular change inside brain cells that helps mediate the process.

Led by Sabrina Diano, Ph.D., professor of obstetrics, gynecology & reproductive sciences, of neuroscience, and of comparative medicine, the team focused on pro-opiomelanocortin (POMC) neurons—brain cells known to regulate energy and metabolism. They found that after a meal, POMC neurons in mice had lower levels of the protein DRP1. DRP1 regulates mitochondrial fission, controlling the size and number of energy-generating mitochondria inside cells. In mice that had been fed, mitochondria became larger. In mice that were fasting, DRP1 levels rose, causing mitochondria to undergo fission and become smaller.

The change, the researchers reported on Feb. 9 in Cell Metabolism, is crucial to how the brain responds to blood sugar levels and sends signals throughout the body to coordinate a response to meals or fasting. Altered mitochondria in the brain, they hypothesize, could even be a source of complications that arise from certain treatments for diabetes, though more study is necessary.


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