Mice who were genetically engineered to lack the gene for Crat showed higher-than-normal rates of converting stored forms of fuel molecules into ready-for-consumption glucose during a phase of food restriction. The mice also displayed increased fatty acid metabolism in the liver.
After the mice were allowed to feed freely again, mice without Crat continued to burn fat, whereas normal mice quickly began to only metabolize the incoming glucose from their food.
“Our current studies suggest that Crat affects AgRP neuronal function predominantly during fasting and the transition to refeeding,” the authors write. “Beyond calorie intake, it is becoming clear that the inappropriate handling of nutrient 'fate' is largely responsible for metabolic disease, and this study shows that Crat in AgRP neurons has an unappreciated role in this process.”
Of course, future investigations will need to prove that the same pathway occurs in humans, something that is not as definite as some headline-grabbing research would lead you to believe. But if a similar process does occur in human AgRP cells, the team is optimistic about potential applications.
"Manipulating this protein offers the opportunity to trick the brain and not replace the lost weight through increased appetite and storage of fat," Andrews said in a statement.