Table 5 Key mechanisms of antihyperglycaemic agents

Delay gastric emptying

Slows the passage of food from the stomach into the small intestine thereby slowing the absorption of glucose

Usually achieved via the activation of the GLP1 receptor, or the inhibition of DPP-4

[118, 119]

Enzyme inhibition

Inhibition of carbohydrate digesting enzymes (e.g. alpha-amylase and alpha-glucosidase) slows release of glucose from digested food

Inhibition of enzymes involved in hepatic glucose metabolism (e.g. glucose-6-phosphatase) or reduces hepatic glucose output

[120,121,122]

Insulin secretagogue activity

Stimulates insulin secretion from pancreatic β-cells

[82]

Insulin-like/insulin sensitizing activity

Enhances glucose uptake by target tissue by stimulating the cell surface expression of GLUT transporters (liver, adipose tissue, and skeletal muscle)

[84]

Reduce intestinal glucose uptake

Reduce absorption of glucose from digested food and into the blood stream either through direct inhibition of enterocyte SGLT-1 or GLUT-2 transporter proteins

[123]

Reduce glucose reabsorption in the kidney

Increases the amount of glucose excreted in urine by inhibiting SGLT-2 proteins in the kidneys which prevents the reabsorption of glucose into the blood stream

[50,51,52]