ROS-mediated glucose metabolic reprogram induces insulin resistance in type 2 diabetes

Dong, Kelei; Ni, Hua; Wu, Meiling; Tang, Ziqing; Halim, Michael; Shi, Dongyun

doi:10.1016/j.bbrc.2016.05.087

Cited by 60 publications

(36 citation statements)

References 24 publications

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“…The protocol of the induction of diabetes type 2 was performed according to the method described by Dong et al (12) with minor modifications. In brief, the 30 animals of the diabetes group followed a 12-h fasting period, and subsequently a combinational procedure which included a single injection with streptozotocin (40 mg kg -1 ) i.p.…”

Section: Methodsmentioning

confidence: 99%

Oxidative Stress Alterations in the Bladder of a Short-period Type 2 Diabetes Rat Model: Antioxidant Treatment Can Be Beneficial for the Bladder

Tsounapi

Honda

Hikita

et al. 2019

In Vivo

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Background/Aim: A short-period type 2 diabetes model was established in order to identify changes in oxidative stress in the bladder at the initiation of the disease. The effect of antioxidant treatment was examined. Materials and Methods: Diabetes was induced in adult male Wistar rats with a single dose of streptozotocin (40 mg/kg; i.p.). Diabetic animals were then randomly separated into three groups: No treatment (DM), resveratrol treatment, and taurine treatment, and fed with a high-fat diet. Age-matched non-diabetic animals were used and fed with normal diet (control). Two weeks later, animals were sacrificed and bladders were processed for histological evaluation, and further analysis for oxidative stress markers. Results: The body weight of all diabetic animals was significantly lower compared to the controls. The DM group demonstrated a significantly higher bladder weight to body weight ratio compared to the control. The bladder in the DM group demonstrated abruption of the mucosa from the muscularis and edema in the transitional epithelium. Bladders from the resveratrol-, and taurinetreated groups did not demonstrate these histological alterations. The level of malondialdehyde (MDA) in the bladder was significantly higher in the DM group compared to all other groups. Immunohistochemistry showed that diabetes induced a moderate to strong expression of oxidative stress markers MDA and 4-hydroxynonenal, and DNA oxidative stress marker 8-deoxyguanosine in the DM group compared to the other groups. Conclusion: Prompt diagnosis and treatment of diabetes is crucial in regard to disease progression. Specifically, in the bladder it appears that both mild damage at the structural level, as well as oxidative damage at the molecular level may be prevented by antioxidant treatment.

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Section: Methodsmentioning

confidence: 99%

Oxidative Stress Alterations in the Bladder of a Short-period Type 2 Diabetes Rat Model: Antioxidant Treatment Can Be Beneficial for the Bladder

Tsounapi

Honda

Hikita

et al. 2019

In Vivo

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“…In addition, insulin could also regulate PPP and further stimulate glucose metabolism . Aberrant PPP metabolism has been identified in various models of diabetes, leading to insulin resistance, dysregulation of lipid metabolism, oxidative stress, and inflammation . For example, glucose‐6‐phosphate dehydrogenase (G6PD) is highly expressed in the adipose tissues of subjects with obesity and diabetes, which catalyzes glucose and glucose‐6‐phophate dehydrogenation to form NADPH and 6‐phosphogluconlactone.…”

Section: Mr and Diabetesmentioning

confidence: 99%

Metabolic Regulation of Methionine Restriction in Diabetes

Yin

Ren

Chen

et al. 2018

Molecular Nutrition Food Res

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Although the effects of dietary methionine restriction have been investigated in the physiology of aging and diseases related to oxidative stress, the relationship between methionine restriction (MR) and the development of metabolic disorders has not been explored extensively. This review summarizes studies of the possible involvement of dietary methionine restriction in improving insulin resistance, glucose homeostasis, oxidative stress, lipid metabolism, the pentose phosphate pathway (PPP), and inflammation, with an emphasis on the fibroblast growth factor 21 and protein phosphatase 2A signals and autophagy in diabetes. Diets deficient in methionine may be a useful nutritional strategy in patients with diabetes.

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“…Excessive ROS are involved in the multifactorial etiology of insulin resistance and the subsequent development of T2D [9]. Oxidative stress alters the insulin receptor and the insulin receptor substrate (IRS) signaling pathway via kinase activity (serine/threonine), leading to multi-site phosphorylation [10]. These events increase serine IRS phosphorylation and decrease thyrosine, leading to insulin resistance [11].…”

Section: Introductionmentioning

confidence: 99%

Trace Elements Modulates Oxidative Stress in Type 2 Diabetes

Gouaref¹,

Koceir²

2018

Diabetes Food Plan

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The relationship between antioxidant trace elements (ATE) and metabolic disease is subtle and complex due to overproduction of reactive oxygen species (ROS). In type 2 diabetes (T2D), the relationship between ATE and insulin-like trace elements is very complex during oxidative stress (OS), being mediated by hyperglycemia, dyslipidemia and inflammation. The important role assigned to ATE (zinc, selenium, copper, manganese and chromium) by their involvement at different levels: Hemodynamic homeostasis (endothelial function and protein glycation), energy metabolism (carbohydrate and lipid tolerance) and enzymatic antioxidant protection [superoxide dismutase (SOD), glutathione peroxidase (GPx)]. The ROS-mediated cellular signaling process is crucial. Manganese and selenium levels abnormalities might to be useful indicators of oxidative damage. Two major factors were suggested: lack of Mn bioavailability leading to the decrease of mitochondrial SOD activity (cytosolic SOD remains active), and low blood selenium level implying a decrease in GPx activity. In T2D pathophysiology, it appears that antioxidant defense is preserved in the cytosol (Cu/Zn-SOD) in T2D, whereas it is impaired in mitochondria (Mn-SOD) in the three pathologies, which make this cell organelle a true ATE therapeutic target. Future challenges require the in-depth investigations of mitochondrial mechanisms, involved the antioxidant trace elements signaling pathways in T2D pathophysiology.

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ROS-mediated glucose metabolic reprogram induces insulin resistance in type 2 diabetes

Cited by 60 publications

References 24 publications

Oxidative Stress Alterations in the Bladder of a Short-period Type 2 Diabetes Rat Model: Antioxidant Treatment Can Be Beneficial for the Bladder

Oxidative Stress Alterations in the Bladder of a Short-period Type 2 Diabetes Rat Model: Antioxidant Treatment Can Be Beneficial for the Bladder

Metabolic Regulation of Methionine Restriction in Diabetes

Trace Elements Modulates Oxidative Stress in Type 2 Diabetes

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