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Diabetesmellitus is a metabolic disorder constituting a majorhealth problem whose prevalence has gradually increased worldwideover the past few decades. Type 2 diabetes mellitus (T2DM) remainsmore complex and heterogeneous and arises as a combination of insulinresistance and inadequate functional β-cell mass and comprisesabout 90% of all diabetic cases. Appropriate experimental animal modelsare essential for understanding the molecular basis, pathogenesisof complications, and the utility of therapeutic agents to abrogatethis multifaceted disorder. Currently, animal models for T2DM areobtained as spontaneously developed diabetes or diabetes induced bychemicals or dietary manipulations or through surgical or geneticmethods. The currently used diabetogenic agents have certain limitations.Recently, methylglyoxal (MG), a highly reactive compound derived mainlyfrom glucose and fructose metabolism has been implicated in diabeticcomplications. MG is a major precursor of the advanced glycation endproduct (AGE) and promotes impaired functions of insulin signaling,GLUT transporters, anion channels, kinases, and endothelial cellsand is finally involved in apoptosis. Recent array of literature alsocited that higher concentrations of MG causes rapid depolarization,elevated intracellular Ca2+concentration, and acidificationin pancreatic β-cells. This review henceforth highlights themechanism of action of MG and its implications in the pathophysiologyof experimental diabetes. [ABSTRACT FROM AUTHOR]