Advanced glycation end products upregulate insulin receptor substrate-1 (IRS-1) in granulosa cells

Merhi, Zaher; Thornton, Kim L.; Bennett-Toomey, Jill; Hennebold, Jon D.; Büyük, Erkan

doi:10.1016/j.fertnstert.2017.07.102

Cited by 2 publications

(3 citation statements)

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“…There is growing evidence that SGLT2i improve redox state in the diabetic milieu [92]. They can exert potent antioxidative properties by several molecular mechanisms including improvement in mitochondrial dysfunction [92,93], regulating the RAS (renin-angiotensin system) activity [70,94], attenuating inflammation-induced free radical generation [95,96], lowering the AGEs (advanced glycation end products) and AGE/RAGE (receptors for advanced glycation end products) crosstalk [97,98], down-regulating the pro-oxidant enzymes expression/activity as NADPH (Nicotinamide adenine dinucleotide phosphate) oxidase, eNOS (endothelial nitric oxide synthase) and xanthine oxidase [99,100]. Based on this evidence, SGLT2 inhibition ameliorates oxidative stress and could improve insulin sensitivity by attenuating oxidative damages in the diabetic milieu [57,101].…”

Section: Reduction In Oxidative Stressmentioning

confidence: 99%

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Molecular mechanisms by which SGLT2 inhibitors can induce insulin sensitivity in diabetic milieu: A mechanistic review

et al. 2020

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Sodium-glucose co-transporter-2 inhibitors (SGLT2i) are a relatively newer class of antihyperglycemic medications that reduce blood glucose by inhibition of renal glucose re-uptake, thereby increasing urinary glucose excretion. Although glycosuria is the primary mechanism of action of these agents, there is some evidence suggesting they can reduce insulin resistance and induce peripheral insulin sensitivity. Identifying the molecular mechanisms by which these medications improve glucose homeostasis can help us to develop newer forms of SGLT2i with lesser side effects. We have reviewed the molecular mechanisms and signaling pathways by which SGLT2i therapy improve insulin sensitivity and ameliorates insulin resistance.

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Section: Reduction In Oxidative Stressmentioning

confidence: 99%

“…Reduce insulin resistance by attenuating the oxidative stress-dependent IST impairment [57,70,89,94,97,98,101]…”

Section: Reducing the Oxidative Stressmentioning

confidence: 99%

Molecular mechanisms by which SGLT2 inhibitors can induce insulin sensitivity in diabetic milieu: A mechanistic review

et al. 2020

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“…Advanced glycation end products (AGEs), a major source of freeradical production (Nowotny, Jung, Höhn, Weber, & Grune, 2015) in diabetes, in particular, may increase their damage (Saremi et al, 2017). Hyperglycemia is a potent stimulator for generating AGEs and intensifies the AGEs-RAGEs (receptor for AGEs) crosstalk that increases free-radical production (Yamagishi, 2018); lowering the blood glucose decreases AGE production and therefore free-radical generation (Merhi, Thornton, Bennett-Toomey, Hennebold, & Buyuk, 2017). Maeda, Matsui, Takeuchi, and Yamagishi (2013) demonstrated that SGLT2 inhibitors induced normoglycemia, thus decreasing AGE generation with a reduction in oxidative stress, and empagliflozin improved cardiac function by reducing AGE generation and lowering oxidative damage (Table 2; Habibi et al, 2017).…”

Section: Sglt2 Inhibitors and Free-radical Generationmentioning

confidence: 99%

Sodium–glucose cotransporter inhibitors and oxidative stress: An update

Yaribeygi

Atkin

Butler

et al. 2018

Journal Cellular Physiology

120

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Sodium-glucose cotransporter 2 (SGLT2) inhibitors are therapeutic agents that have been used recently to reduce tubular absorption of glucose, leading to enhanced glycosuria, resulting in the reduction of blood glucose and improved diabetes control.Recent data suggest that SGLT2 inhibitors have antioxidant properties that may be key to the reduction in cardiovascular death found in clinical trials. Oxidative stress is involved in the development and progression of atherosclerosis, as well as underlying diabetes complications, and may result from either increased free-radical production, a reduction in antioxidative capacity, or a combination of both. In this report, we have reviewed the recent evidence of the impact that SGLT2 inhibition may have on improved oxidative stress by either amelioration of free-radical generation or potentiation of cellular antioxidative capacity, and its importance in the prevention of cardiovascular and diabetes complications.

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Advanced glycation end products upregulate insulin receptor substrate-1 (IRS-1) in granulosa cells

Cited by 2 publications

References 0 publications

Molecular mechanisms by which SGLT2 inhibitors can induce insulin sensitivity in diabetic milieu: A mechanistic review

Molecular mechanisms by which SGLT2 inhibitors can induce insulin sensitivity in diabetic milieu: A mechanistic review

Sodium–glucose cotransporter inhibitors and oxidative stress: An update

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