Regular Physical Exercise as a Strategy to Improve Antioxidant and Anti-Inflammatory Status: Benefits in Type 2 Diabetes Mellitus

Lemos, E. Teixeira de; Oliveira, Jorge; Pinheiro, João Páscoa; Reis, Flávio

doi:10.1155/2012/741545

Cited by 80 publications

(51 citation statements)

References 155 publications

(155 reference statements)

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“…The present study showed that Celastrol promoted mitochondrial biogenesis and inhibited mitochondrial ROS production. Chronic inflammatory cytokines are also potent stimulators of ROS production, and ROS can induce oxidative stress, with the subsequent activation of inflammatory pathways and mitochondrial damage [31], [32], [33]. Previous studies have shown that Sirt1 has a regulatory effect on oxidative stress in many tissues through reducing the ROS levels and improving cell survival via this antioxidant effect [34].…”

Section: Discussionmentioning

confidence: 99%

Celastrol ameliorates liver metabolic damage caused by a high-fat diet through Sirt1

Zhang

Geng

Liu

et al. 2017

Molecular Metabolism

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ObjectiveCelastrol was recently identified as a potential novel treatment for obesity. However, the effect of Celastrol on nonalcoholic fatty liver disease (NAFLD) remains elusive. The aim of this study is to evaluate the role of Celastrol in NAFLD.MethodsFunctional studies were performed using wild-type C57BL/6J (WT) mice and liver specific Sirt1-deficient (LKO) mice. The molecular mechanism was explored in primary mouse liver and primary hepatocytes.ResultsWhen WT mice receiving a high-fat diet (HFD) were treated with Celastrol, reductions in body weight, subcutaneous and visceral fat content, and liver lipid droplet formation were observed, along with reduced hepatic intracellular triglyceride and serum triglyceride, free fatty acid, and ALT concentrations. Furthermore, Celastrol decreased hepatic sterol regulatory element binding protein 1c (Srebp-1c) expression, enhanced the phosphorylation of hepatic AMP-activated protein kinase α (AMPKα), and increased the expression of hepatic serine–threonine liver kinase B1 (LKB1). Additionally, Celastrol treatment improved glucose tolerance and insulin sensitivity in WT mice fed the HFD. Celastrol administration also improved the anti-inflammatory and anti-oxidative status by inhibiting nuclear factor kappa B (NFκB) activity and the mRNA levels of proinflammatory cytokines and increasing mitochondrial DNA copy number and anti-oxidative stress genes expression in WT mice liver, in vivo and in vitro. Moreover, Celastrol induced hepatic Sirt1 expression in WT mice, in vivo and in vitro. These Celastrol-mediated protective effects in WT mice fed a HFD were abolished in LKO mice fed a HFD. It was more interesting that Celastrol aggravated HFD-induced liver damage in LKO mice fed a HFD by inhibiting the phosphorylation of AMPKα and boosting the translocation of NFκB into the nucleus, thereby resulting in the increase of Srebp-1c expression and the mRNA levels of liver proinflammatory cytokines.ConclusionsCelastrol ameliorates NAFLD by decreasing lipid synthesis and improving the anti-oxidative and anti-inflammatory status. And Sirt1 has an important role in Celastrol-ameliorating liver metabolic damage caused by HFD.

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Section: Discussionmentioning

confidence: 99%

Celastrol ameliorates liver metabolic damage caused by a high-fat diet through Sirt1

Zhang

Geng

Liu

et al. 2017

Molecular Metabolism

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“…Increased physical activity and weight loss are associated with lower CRP and reduction in concentration of other markers of inflammation3392. Therefore, both intervention alone or in combination might act through AMPK pathway and inhibit the activation of downstream inflammation through inhibition of CRP and NFκB.…”

Section: Discussionmentioning

confidence: 99%

“…Regular exercising affects the regulation of enzymatic antioxidants such as catalase, super oxide dismutase and non-enzymatic antioxidants including vitamin E and C. Regular exercise is linked to CRP reduction, lipid profile regulation, increase of nitric oxide synthase, improvement in insulin sensitivity, and preservation of beta cell mass. Thus regular exercise leads to the adaptation in antioxidant capacity, protecting cells against harmful effects of oxidative stress33.…”

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confidence: 99%

Purslane (Portulaca oleracea) Seed Consumption And Aerobic Training Improves Biomarkers Associated with Atherosclerosis in Women with Type 2 Diabetes (T2D)

Dehghan

Soori

Gholami

et al. 2016

Sci Rep

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The aim of this study was to investigate the responses of atherosclerosis plaque biomarkers to purslane seed consumption and aerobic training in women with T2D. 196 women with T2D were assigned into; (1) placebo (PL), (2) aerobic training+placebo (AT + PL), 3) purslane seeds (PS), aerobic training+purslane seeds (AT + PS). The training program and purslane seeds consumption (2.5 g lunch and 5 g dinner) were carried out for 16 weeks. The components of purslane seed were identified and quantified by GC–MS. Blood samples were withdrawn via venipuncture to examine blood glucose, low-density lipoprotein (LDL), high-density lipoprotein (HDL), cholesterol, triglycerides (TG), creatinine, urea, uric acid, NF-κB, GLP1, GLP1R, TIMP-1, MMP2, MMP9, CRP, CST3, and CTSS expressions. Blood glucose, LDL, cholesterol, TG, creatinine, urea, and uric acid levels in the (P), (AT), and (AT + PS) groups were significantly decreased compared to the pre-experimental levels or the placebo group, while HDL, significantly increased. Furthermore, the protein and mRNA levels of NF-κB, TIMP-1, MMP2 &9, CRP, CST3, and CTSS in the (P), (AT), (AT + PS) significantly decreased compared to pre-experimental or the placebo group, while level of GLP1 and GLP1-R increased drastically. Findings suggest that purslane seed consumption alongside exercising could improve atherosclerosis plaque biomarkers through synergistically mechanisms in T2D.

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“…Although a vast amount of research has been conducted to understand the mechanism by which exercise alters the development of obesity and T2D, its effects on glucose-induced insulin secretion by β-cells is poorly understood. In terms of pancreatic function, experiments in humans and animals have variously demonstrated that exercise improves insulin resistance, increases insulin sensitivity, increases pancreatic β-cell mass and generally enhances β-cell function and insulinotropic action, especially in T2D patients [6]. However, the glucose responsiveness of the pancreatic islets obtained from trained rats varies according to the protocol (acute or chronic exercise), glucose concentration and metabolic state (diabetic, obese or lean rats).…”

Section: Introductionmentioning

confidence: 99%

Glycolytic and Mitochondrial Metabolism in Pancreatic Islets from MSG-Treated Obese Rats Subjected to Swimming Training

Leite

Ferreira

Rickli

et al. 2013

Cell Physiol Biochem

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Backgrounds/Aims: Obese rats obtained by neonatal monosodium glutamate (MSG) administration present insulin hypersecretion. The metabolic mechanism by which glucose catabolism is coupled to insulin secretion in the pancreatic β-cells from MSG-treated rats is understood. The purpose of this study was to evaluate glucose metabolism in pancreatic islets from MSG-treated rats subjected to swimming training. Methods: MSG-treated and control (CON) rats swam for 30 minutes (3 times/week) over a period of 10 weeks. Pancreatic islets were isolated and incubated with glucose in the presence of glycolytic or mitochondrial inhibitors. Results: Swimming training attenuated fat pad accumulation, avoiding changes in the plasma levels of lipids, glucose and insulin in MSG-treated rats. Adipocyte and islet hypertrophy observed in MSG-treated rats were attenuated by exercise. Pancreatic islets from MSG-treated obese rats also showed insulin hypersecretion, greater glucose transporter 2 (GLUT2) expression, increased glycolytic flux and reduced mitochondrial complex III activity. Conclusion: Swimming training attenuated islet hypertrophy and normalised GLUT2 expression, contributing to a reduction in the glucose responsiveness of pancreatic islets from MSG-treated rats without altering glycolytic flux. However, physical training increased the activity of mitochondrial complex III in pancreatic islets from MSG-treated rats without a subsequent increase in glucose-induced insulin secretion.

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Regular Physical Exercise as a Strategy to Improve Antioxidant and Anti-Inflammatory Status: Benefits in Type 2 Diabetes Mellitus

Cited by 80 publications

References 155 publications

Celastrol ameliorates liver metabolic damage caused by a high-fat diet through Sirt1

Celastrol ameliorates liver metabolic damage caused by a high-fat diet through Sirt1

Purslane (Portulaca oleracea) Seed Consumption And Aerobic Training Improves Biomarkers Associated with Atherosclerosis in Women with Type 2 Diabetes (T2D)

Glycolytic and Mitochondrial Metabolism in Pancreatic Islets from MSG-Treated Obese Rats Subjected to Swimming Training

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