A research group led by Professor Keiichi Nakayama of Kyushu University, Assistant Professor Yasuyuki Kita and Professor Michiko Shirane of Nagoya City University, and Professor Masaaki Nishiyama of Kanazawa University found that CHD8, the causative protein of autism, causes fat differentiation and fat in adipocytes. We have discovered that it has a very important role in the accumulation of drops.It is expected to lead to a new treatment for obesity.
CHD8 is the gene with the highest mutation rate in autistic patients. In autism with a mutation in the CHD8 gene, in addition to the symptoms peculiar to autism such as impaired social interaction (communication) and strong commitment to follow fixed procedures (persistence tendency), lean people It has been reported that there are many.This suggests that the CHD8 protein has important functions not only for neurogenesis but also for metabolic function and fat differentiation, but the specific mechanism remains a mystery.
This time, the research group created a new mouse lacking the CHD8 gene of adipose stem cells (which are located in adipose tissue and have the ability to differentiate into various tissues).As a result, they found that lipid differentiation and lipid droplet accumulation that promote obesity were suppressed.In addition, when the function of CHD8 in adipocytes was investigated by a new technique called "transomics analysis", CHD8 cooperates with C / EBPβ, a protein important for adipocyte differentiation, and is involved in adipocyte differentiation and lipid droplet accumulation. It was found to regulate the expression of related genes.Furthermore, it was found that artificial deletion of the CHD8 gene in mice makes it difficult to gain weight even when eating a high-fat diet.
These results indicate that obesity can be treated by suppressing CHD8 only in adipose tissue, and the development of a new treatment for obesity is expected.
Paper information:[Cell Reports] The Autism-Related Protein CHD8 Cooperates with C / EBPβ to Regulate Adipogenesis
