Figure 4.

Representative image delineating the plausible anti-diabetic effect of CM. Food breakdown in the gastrointestinal tract (GI) leads to release of gut hormones, such as Glucagon-Like Peptide-1 (GLP-1) and Glucose Dependent Insulinotropic Polypeptide (GIP), which seemingly stimulate glucose-dependent insulin secretion by the pancreatic Beta cells. Insulin thereby promotes glucose uptake by the insulin sensitive tissues. Mechanistically, insulin, upon binding to insulin receptors, initiates a signaling cascade that eventually induces translocation of glucose receptors (GLUTs) to the membrane whereby glucose can be up-taken. These gut hormones are cleaved by DPP-IV enzymes which leads to attenuation of insulin secretion. Interestingly, CM and its constituents have been reported to activate GLP1/GIP and inhibit Dipeptidyl peptidase-IV (DPP-IV), activate insulin receptor and inhibit glucagon receptor. Additionally, it has been reported that CM embodies insulin-like peptides that mimic insulin responses, another aspect adding to their anti-diabetic potential.