Role of Galectin-3 in Obesity and Impaired Glucose Homeostasis

Abstract EN

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.