Galectin-3 is an important modulator of several biological functions. It has been implicated in numerous disease conditions, particularly in the long-term complications of diabetes because of its ability to bind the advanced glycation/lipoxidation end products that accumulate in target organs and exert their toxic effects by triggering proinflammatory and prooxidant pathways. Recent evidence suggests that
galectin-3 may also participate in the development of
obesity and
type 2 diabetes. It has been shown that
galectin-3 levels are higher in obese and diabetic individuals and parallel deterioration of
glucose homeostasis. Two studies in
galectin-3 knockout mice fed a high-fat diet (HFD) have shown increased adiposity and adipose tissue and systemic
inflammation associated with altered
glucose homeostasis, suggesting that
galectin-3 negatively modulates the responsiveness of innate and adaptive immunity to
overnutrition. However, these studies have also shown that impaired
glucose homeostasis occurs in
galectin-3 knockout animals independently of
obesity. Moreover, another study reported decreased weight and fat mass in HFD-fed
galectin-3 knockout mice. In vitro,
galectin-3 was found to stimulate differentiation of preadipocytes into mature adipocytes. Altogether, these data indicate that
galectin-3 deserves further attention in order to clarify its role as a potential player and therapeutic target in
obesity and
type 2 diabetes.