Nuclear translocation of STAT3 by in vitro metreleptin administration causes lipolysis in human primary adipocytes

Abstract

We utilized subcutaneous (SC)- and omental (OM)-derived human primary adipocytes (hPA) from obese male, and investigated whether synthetic analog of leptin, metreleptin, may regulate lipolysis via translocation of STAT3 to the nucleus. We observed that 50 ng/mL of metreleptin increases STAT3 phosphorylation in both SC- and OM-derived hPA. Importantly, we found for the first time that metreleptin is capable of trans-locating STAT3 to the nucleus and STAT3 blockade inhibits metreleptin-induced lipolysis. Our initial data provide novel insights into the role of STAT3 as probable mediator of the action of metreleptin in regulating metabolism.