"Professor Kim Jae-woo’s Research Team Finds a Critical Mediator of glucocorticoid in Adipogenesis"
Identification of Obesity-associated Protein, Dexras1
This study, collaborated with Dr. Solomon H. Snyder in Johns Hopkins University, has been recently published in the Proceedings of the National Academy of Sciences in the United States of America (PNAS). They identified Dexras1 as a new gene involved in adipocyte differentiation, and this discovery has the potential to lead Dexras1 as a target molecule in the treatment of obesity as well as Cushing’s syndrome. An excessive level of adipogenesis potentially causes obesity, a strong risk factor for metabolic diseases, and glucocorticoid has a role in fat deposition and adipocyte differentiation. However, its mechanism has been barely known.
According to the results using 3T3-L1 pre-adipocyte model, in which glucocorticoid is necessary for the differentiation, Prof. Kim and Dr. Kim Hyo Jung (Yonsei University College of Medicine) in his laboratory found that Dexras1 is expressed in response to glucocorticoid and acts as a critical mediator of this hormone. Without Dexras1, adipogenesis is significantly impaired. Using Dexras1 knockout mice, they also found that the weight gain in Dexras1 knockout mice was significantly less than that in wild type mice, with no significant change in the amount of food intake and exercise. Moreover, visceral fat mass and the size of adipocytes were markedly reduced, and the insulin resistance and blood sugar level were also improved in the knockout mice.
Prof. Kim noted that this result provides an answer for a long standing question about the mechanism of metabolic effect of glucocorticoid. It will improve the situation we are facing now in terms of curing metabolic syndrome including obesity. Moreover, it has a value since it proposes a novel target molecule which can be used in the treatment of diseases related to metabolic imbalance due to the over-production of steroid like Cushing’s syndrome.