When warm-blooded animals, including humans, are exposed to a cold environment for a long time, the quality of adipose tissue changes from "white adipocytes" that store energy as fat to "beige adipocytes" that consume fat and produce heat. It has a mechanism to change
Since beige adipocytes actively burn fat, they are attracting attention as a new therapeutic and preventive strategy for obesity.However, the details of the intracellular signal transduction mechanism that induces beige have not been clarified so far.
A research group led by Professor Toshiro Sakai of Tohoku University Graduate School of Medicine/The University of Tokyo Research Center for Advanced Science and Technology has developed β-AR, which activates protein kinase (PKA) when the brain senses a cold stimulus. We clarified the mechanism by which -PKA signaling induces beige adipocytes by inhibiting the activity of protein phosphatase (MYPT1-PP1β).Normally, MYPT1-PP1β suppresses beige adipocyte induction by integrally controlling transcriptional regulation by epigenome rewriting enzymes and transcription factors.However, under cold stimulation, PKA activated by β-AR-PKA signaling suppresses the action of MYPT1-PP1β. It is said that he found that he was induced.
Adipose tissue-specific MYPT1-deficient mice showed marked induction of beige adipogenesis, and were less likely to gain weight and develop glucose intolerance even when fed a high-fat carbohydrate diet.The results of this research are expected to be applied to new treatment and prevention methods for lifestyle-related diseases such as obesity and diabetes.
Paper information:[Nature Communications] MYPT1-PP1β phosphatase negatively regulates both chromatin landscape and coactivator recruitment for beige adipogenesis