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Table 6 Enzyme targets for antidiabetic therapy

From: Understanding glycaemic control and current approaches for screening antidiabetic natural products from evidence-based medicinal plants

Enzyme Function Effect of inhibition References
α-Amylase Hydrolysis of starch to oligosaccharides in the mouth and small intestine Delays carbohydrate digestion → slower absorption of glucose from small intestine → reduces postprandial hyperglycaemia [165, 168]
α-Glucosidase Hydrolysis of oligosaccharides and sucrose to glucose in the small intestine Delays carbohydrate digestion → slower absorption of glucose from small intestine → reduces postprandial hyperglycaemia [165, 168]
Glucose-6-phosphatase Dephosphorylation of glucose-6-phosphate to produce glucose (rate-limiting step in gluconeogenesis) Prevents the increase of BGLs during the fasted state by inhibiting gluconeogenic glucose synthesis [166]
PTP-1B (protein tyrosine phosphatase-1B) Dephosphorylation of insulin receptor, and insulin receptor substrates 1 and 2 Enhances insulin receptor and IRS-1/IRS-2 phosphorylation → increase translocation of glucose transporters for glucose uptake → reduce BGL [167]
DPP-4 (dipeptidyl peptidase-4) Breakdown of GLP-1 Increases the level of endogenous GLP-1 → lowers production of glucagon and increases insulin production → lowering of BGLs postprandially [47, 167, 169]