Obesity is a risk factor for metabolic diseases, posing a substantial therapeutic challenge towards obesity-related diseases and a large economic burden on the health care. Despite the potentially huge market, a truly effective and safe therapy for obesity and associated maladies is elusive. Cyclin-dependent kinase 6 (CDK6) plays an important function in metabolism. Differing from its homolog Cyclin-dependent kinase 4 (CDK4), CDK6 is less universally expressed, which makes CDK6 as a unique potential therapeutic target for many diseases. By using our Cdk6 mouse models, we have found that CDK6 induces obesity by negatively regulating beige cell formation and de novo lipogenesis in adipose tissues but not in the liver, positively promoting differentiation of white adipocytes from stem cells, and accelerating insulin resistance and glucose intolerance. Therefore, inhibition of CDK6 kinase activity pharmaceutically can protect individuals from obesity and obesity associated maladies.

Miaofen g Hu has completed her PhD from Boston University School of Medicine and postdoctoral studies from Harvard University School of Medicine. She has published more than 34 papers in reputed journals and has been serving as an editorial board member of different journals including Clinical Diabetes, Current Advances in Oncology Research, and Open Access Journal of Hematology.