Skip to content
Phone: 301-655-1084 Email:

 In the United States, diabetes is now the third leading cause of death (0.33 million) after heart disease and cancer. Type 2 diabetes (T2D), which accounts for about 90% of all diabetes, is often associated with obesity. It happens when the pancreas doesn’t release enough of the hormone, insulin, or the body’s cells don’t react to insulin. Obesity-associated insulin resistance is a hallmark of T2D and plays a central role in metabolic syndrome. Obesity-induced inflammation and insulin resistance mediated by macrophages and other immune cells are well connected.

Despite many drugs available to treat T2D, no FDA-approved drugs directly work on the insulin receptor (IR) to overcome insulin resistance. Recent studies show that macrophage-derived galectin-3 can bind directly to the IR and inhibit downstream IR signaling causing insulin resistance and impaired glucose tolerance in obesity-induced T2D (see Figure 5). Gal3 is also known to amplify beta-cell apoptosis and islet inflammation in T2D. Administration of galectin-3 to mice causes insulin resistance and glucose intolerance, whereas inhibition of galectin-3, through either genetic or pharmacologic loss of function, improved insulin sensitivity in obese mice. These fundamental observations elucidate a novel role of Gal3 that promotes obesity-mediated inflammation (macrophage-derived galectin-3) and insulin resistance and suggest that specific inhibition of galectin-3 may represent a promising therapeutic strategy to restore insulin sensitivity.

At GlycoMantra, we have shown in relevant animal model that our drug GM101 improves glucose tolerance and insulin sensitivity.

Figure 5

Figure 5. Role of Galectin-3 in the Promotion of Insulin Resistance in Type 2 Diabetes.

Relevant Publications:

  1.  Li P, Liu S et al: Hematopoietic-Derived Galectin-3 Causes Cellular and Systemic Insulin Resistance. Cell 2016, 167:973-984. [PubMed]

  1. Petrovic I, Pejnovic N et al: Overexpression of galectin 3 in pancreatic cells amplifies b-cell apoptosis and islet inflammation in type-2 diabetes in mice. Front. Endocrinol. 2020, 11:30 [PubMed]

Contact us
Back To Top