Ablation of Galectin-1 Reduces Adipogenesis and Obesity

Abstract

Galectin-1 is a member of the animal lectin family that contains a carbohydrate-recognition binding domain (CRD) that binds a B-galactoside. Many studies are reported about the role of galectin-1 in cancer and immune disorders. But, the role of galectin-1 in metabolic dysfunction is not fully understood. We were interested in the role of galectin-1 on metabolic diseases and investigated the mechanism how galectin-1 regulates adipocyte differentiation and high fat diet (HFD) induced obesity. The level of galectin-1 increased during adipocyte differentiation and was predominantly expressed in mouse fat tissues. Galectin-1 knockdown significantly reduced adipocyte differentiation in 3T3-L1 cells and also decreased the expression of peroxisome proliferator-activated receptor (PPAR)-γ, ccaat enhancer binding protein (C/EBP)-α. fatty acid binding protein (FABP) 4 and fatty acid synthase (FASN). When lactose was treated to inhibit function of extracellular galectin-1, there was no effect on adipocyte differentiation. After 10-week high-fat diet (60% fat), lgals1-/- mice had lower body weight and WAT mass than wild type (lgals1+/+) mice. The expression levels of lipogenic genes were significantly down-regulated in liver and gonadal WAT of lgals1-/- mice. In addition, lgals1-/- mice had elevated expression of genes involved in thermogenesis in inguinal WAT and BAT. These data suggest that galectin-1 is an important regulator of adipogenesis. We also suppose that galectin-1 might be potential therapeutic target in obesity and fat liver diseases and further study is needed for clinical application. Disclosure J. Baek: None.