Review Article

Role of Galectin-3 in Obesity and Impaired Glucose Homeostasis

Figure 3

Summary of results of animal studies on the role of galectin-3 in obesity and adipogenesis. Structural and molecular features of adipose tissue of galectin-3 knockout mice, either fed with NFD or HFD. With NFD, galectin-3 ablation is associated with increased adiposity. However, fat cell size is not increased and PPARγ expression is even reduced. With HFD, there are contrasting results on the effect of galectin-3 ablation on fat mass and body weight. However, galectin-3 ablation is always associated with defective size and/or impaired ability of adipocytes to respond with an enlargement to the fat overload. These structural features, together with defects in the expression of adipogenic and lipogenic markers (PPARγ and ATGL), suggest a regulatory role for galectin-3 in adipogenesis. Gal-3 = galectin-3; crossed Gal-3 = galectin-3 ablation; NFD = normal-fat diet; HFD = high-fat diet; PPARγ = peroxisome-proliferator-activated receptor γ; ATGL = adipose triacylglycerol lipase.