Scientists have found a switch that controls calorie burning: GPR3. Overexpression of GPR3 in gene-edited mice allows them to maintain metabolic health despite a high-calorie diet! By genetically modifying the mice to increase the expression of GPR3 receptors on the surface of brown fat cells, they found that these mice remained non-obese even when eating a high-calorie diet. These mice burned more energy, gained less fat and were better able to control their blood sugar levels than the control group. Brown fat is a special type of fat that has a strong ability to burn calories. When humans are in a cold environment, these fats will be activated to generate heat and help us get through the difficult times. In cold environments, the level of GPR3 receptors in mice increased significantly. Increasing the level of GPR3 receptors on the surface of brown fat cells can also counteract metabolic diseases in mice that have already become obese. Because of a magical property of GPR3, regulating this receptor is expected to be better than other weight loss drugs. It promotes fat burning by activating certain receptors on the surface of cells. But this also has its shortcomings, because once the medication is stopped, the fat burning process will also stop. Therefore, “the medicine cannot be stopped”! If this drug were on the market, would you like to regulate your obesity switch? Olivia Sveidahl Johansen et al., (2021), Lipolysis drives expression of the constitutively active receptor GPR3 to induce adipose thermogenesis, Cell, DOI: https://doi.org/10.1016/j.cell.2021.04.037 |
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