Obesity and its resulting metabolic syndrome and obesity type 2 diabetes increase the risk of cardiovascular disease, renal disease and malignant tumors, and are major obstacles to extending healthy life expectancy.
In recent years, in addition to the "white adipose tissue" that stores energy, it has been found that "brown adipose tissue" that consumes energy through heat production also exists in human adults, and it is necessary to increase the number and function of brown adipose tissue. Is expected to lead to new treatments for obesity.Meanwhile, a research group at the University of Tokyo revealed that they have succeeded in identifying NFIA (Nuclear factor I-A) as a novel major regulator of brown adipose tissue.
According to the announcement, NFIA activates the brown adipose tissue gene program by binding to the brown adipose tissue-specific open chromatin region (the region where gene transcription takes place) and facilitating information retrieval.In fact, the brown adipose gene program was significantly impaired in NFIA-deficient mice, whereas when NFIA was introduced, activation of the brown adipose gene program was also observed in myoblasts and white adipocytes. Was done.Furthermore, it was found that the NFIA gene was highly expressed in brown adipose tissue of human adults as compared with white adipose tissue, and its expression was positively correlated with the expression of the gene specific to brown adipose.
By enhancing the function of NFIA, it may lead to new treatments for obesity, metabolic syndrome, and obesity type 2 diabetes based on "promotion of energy consumption" instead of "suppression of energy intake".
Paper information:[Nature Cell Biology] NFIA co-localizes with PPARγ and transcriptionally controls the brown fat gene program
