Table 6 Enzyme targets for antidiabetic therapy

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]