I have long standing interest and research experience in specific areas of androgen biology and aging research. For last 16 years of my independent career, I have been interested in delineating the molecular mechanism of androgen action on muscle and fat mass. My initial research work led to the identification of follistatin (Fst) as a novel target of androgen action via activation of Wnt/ß-catenin signaling pathway, and subsequent identification of anabolic pathways that are differentially responsive to testosterone in muscle and prostate tissues.
Using a systematic and comprehensive genetic approach, we identified a novel role of Fst in controlling brown adipose characteristics. My research laboratory demonstrated that Fst over-expression both in-vitro and in-vivo favorably alters lipidomic/metabolomic profiles implicated in lipoprotein and energy metabolism. This work is the first to demonstrate the action of Fst in targeting both browning of white adipose tissue (WAT) and activation of classical brown adipose tissue (BAT) through distinct molecular mechanisms and have tremendous therapeutic potential of Fst for the treatment of obesity and related metabolic syndromes. These novel information regarding potential beneficial effects of Fst has been awarded US patent (US9682093B2) entitled “Composition and Methods for Treating or Preventing Metabolic Syndrome Disorders”. In collaboration with UCLA investigators, we have recently identified a critical role for Fst-induced browning during its antiatherogenic action. Currently, we are investigating the pro-browning and anti-atherogenic role of Fst in details and identifying key molecular targets involved in mitigating dyslipidemia and the development of atherosclerosis using several gain-of-function (adipose-specific Fst transgenic mouse models generated in our laboratory) and loss-of function using Fst-floxed (Fst fl/fl) mouse models. Over the years, my research has been supported by several NIH grants.