Table 2.

Possible molecular pathways by which incretin-based antidiabetic medications protect against oxidative damages (SOD: superoxide dismutase; CAT: catalase; GPX: glutathione peroxidase; Nrf2: nuclear factor erythroid 2-related factor 2; AGEs: advanced glycation end products; Sirt: sirtuin; MDA: malondialdehyde).

	Molecular mechanism	Effects on oxidative stress	Ref.
Direct roles	Antioxidant defense system	Increase expression/activity of antioxidative elements such as SOD, CAT, and GPX at least partly via Nrf2 and Sirt signaling pathways	[60, 68, 69, 73]
	Free radical generation	Reduce the free radical generation thru several pathways such as suppressing prooxidant enzymes and improving mitochondrial function	[54, 60, 86]
Indirect roles	Inflammation-induced oxidative stress	Attenuate procytokines' expression/release leading to inflammation-induced oxidative stress	[49, 54]
	Glucotoxicity	Improve insulin signaling as well as glucose homeostasis leading to lower amount of toxic byproduct as AGEs	[97, 98]
	Lipotoxicity	Reduce lipid metabolites such as MDA due to promoting lipid metabolism	[106–108]