LAUSR

ABSTRACT Adipose tissues, function as energy metabolism and endocrine organ, are closely associated with metabolic diseases such as obesity, insulin resistance and diabetes. Liver kinase B1 (Lkb1) and mechanistic target of rapamycin (mTOR) play crucial roles in regulating energy metabolism and cell growth in adipose tissue. Our recent study generated an adipocyte-specific Lkb1 and mTOR double knockout (DKO) mouse model and found that DKO of Lkb1 and mTOR caused reduction of brown adipose tissue (BAT) and inguinal white adipose tissue (iWAT) mass but increase of liver mass. Moreover, the DKO mice developed fatty liver and insulin resistance but displayed improved glucose tolerance and were resistant to high-fat diet (HFD) -induced obesity. In this commentary, we compare the similarities and differences of the phenotypes found in the DKO mice and Lkb1 or mTOR or mTOR complex 1 (mTORC1) or mTOR complex 2 (mTORC2) single knockout mice. Furthermore, we discuss the potential regulatory mechanism that results in the overlapping or distinct phenotypes found in these models.