The Role of Galectin 3 in the Pathogenesis of Diabetes Mellitus: Focus on Β-Cell Function and Survival

Abstract

Abstract Galectin 3 is a lectin expressed in many tissues with a significant biological role in physiological and pathological processes. Our review aims to sublimate the effects of galectin 3 on the β-cells function and survival. Data about the effect of galectin 3 on β- cells are scarce and contradictory. Several studies have shown that reduced activity of the galectin 3 gene reduces the risk of developing type 1 diabetes in an experimental model of diabetes in galectin 3 deficient mice. On the other side, in an experimental model of type 1 diabetes with mice with selectively enhanced expression of galectin 3 in β-cells, was shown that increased expression of this lectin has a protective role. Unlike type 1 diabetes where the autoimmune process plays a dominant role in pathogenesis, the pathogenesis of type 2 diabetes is multifactorial. One of the main factors which contribute to type 2 diabetes, the insulin resistance, is related to the concentration of soluble galectin 3. The effect of galectin 3 is very important for β-cell function. When a harmful factor acts on a β-cell, its intracellular concentration increases to preserve the function of β-cells and prevent their apoptosis, by blocking the internal path of apoptosis. However, excessive accumulation of galectin 3 inside the cell leads to its secretion, which encourages tissue inflammation. Based on all the above, galectin 3 has a double effect on β-cells.