Alleviation of liver dysfunction, oxidative stress and inflammation underlines the protective effects of polysaccharides from Cordyceps cicadae on high sugar/high fat diet‐induced metabolic syndrome in rats

In a nutshellPotential nutritional influences on sleep apnoea include: overweight, oxidative stress, inflammation, metabolic syndrome and high fat diet.However, so far weight reduction is the only nutritional treatment stemming from this list that is well supported by clinical trials.

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Melatonin protects against cardiac damage induced by a combination of high fat diet and isoproterenol exacerbated oxidative stress in male Wistar rats

Melatonin Research ◽

10.32794/mr11250009 ◽

2019 ◽

Vol 2 (1) ◽

pp. 9-31 ◽

Cited By ~ 1

Author(s):

Auroma Ghosh ◽

Gargi Bose ◽

Tiyasa Dey ◽

Palash Kumar Pal ◽

Sanatan Mishra ◽

...

Keyword(s):

Oxidative Stress ◽

Antioxidant Enzymes ◽

High Fat Diet ◽

Myocardial Damage ◽

Neutrophil Infiltration ◽

Protective Effects ◽

High Fat ◽

Cardiac Damage ◽

Male Wistar Rats ◽

Abnormal Mitochondria

In the current study, it was found that high fat diet (60% of total kCal) (H) or/and isoproterenol (I) exacerbated oxidative stress and caused myocardial damage. This was indicated by increased levels of LPO, PCO, abnormal mitochondria and altered activities of metabolic as well as antioxidant enzymes in myocardium of rats. Melatonin at different doses (10, 20 and 40 mg/kg) effectively protected against myocardial damage induced by H or/and I and preserved all of these altered parameters. Morphological analyses showed that combination of H and I treatment led to the extensive myofibril disintegration and neutrophil infiltration. Melatonin at the dose of 40 mg/kg almost completely prevented these pathological alterations. The mechanistical studies have uncovered that the protective effects of melatonin on the myocardial damage induced by H and I are attributed to its direct and indirect antioxidative capacity, i.e., it directly scavenges free radicals and also regulates the gene expression of antioxidant enzymes. Collectively, based on the evidences gathered from the current study, it will not be unwise to suggest that melatonin can serve as an ideal therapeutic agent for those cardiovascular diseases caused by oxidative stress.

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Protective effects of L-arabinose in high-carbohydrate, high-fat diet-induced metabolic syndrome in rats

Food & Nutrition Research ◽

10.3402/fnr.v59.28886 ◽

2015 ◽

Vol 59 (1) ◽

pp. 28886 ◽

Cited By ~ 16

Author(s):

Lei Hao ◽

Xiaoling Lu ◽

Min Sun ◽

Kai Li ◽

Lingmin Shen ◽

...

Keyword(s):

Metabolic Syndrome ◽

High Fat Diet ◽

Protective Effects ◽

High Fat ◽

High Carbohydrate

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PO-250 Exercise and dietary intervention reduce myocardial oxidative stress in male rats with metabolic syndrome

Exercise Biochemistry Review ◽

10.14428/ebr.v1i5.10983 ◽

2018 ◽

Vol 1 (5) ◽

Author(s):

Chonglin Zhang ◽

Hui Wang ◽

Xiaomin Ding ◽

Shaosheng Liu ◽

Zhi Xia

Keyword(s):

Oxidative Stress ◽

Metabolic Syndrome ◽

Aerobic Exercise ◽

High Fat Diet ◽

Regulatory Factor ◽

High Fat ◽

Model Control ◽

Diet Control ◽

Model Training ◽

Pai 1

Objective Both aerobic exercise and alimentary control relieve oxidative stress (OS). However, there may be different modes. The objective of this study is to identify the effects of OS in metabolic syndrome (MS) rats and explore the mechanisms involved in aerobic exercise and alimentary control. Methods Seventy rats were used. Eight rats were randomly chosen for the control group, while the remaining rats were subjected to MS using a high-fat diet for 18 wk. The MS model rats were subsequently divided into the MHC (model control with high-fat diet), MRC (model control with routine diet), MHE (model training with high-fat diet) and MRE (model training routine diet) groups for 12 wk. The chemotactic factor macrophage chemoattractant protein-1 (MCP-1), the adherence factor plasminogen activator inhibitor I (PAI-1), the oxidative stressor oxidized low density lipoprotein (ox-LDL), and the antioxidative factor endothelial nitric oxide synthase (eNOS) were tested in the serum; moreover, the expressions of MCP-1, PAI-1, and eNOS and the regulatory factor of OS Peroxisome proliferator-activated receptor-alpha (PPARα) were detected in the myocardium. Results OS related markers in serum had changes following the interventions of aerobic exercise and/or diet control. Compared with C, the ox-LDL, MCP-1 and PAI-1 in the MS rats exhibited significant decreases (P＜0.05/0.01), and the eNOS had a significant increase (P＜0.05). Compared with MHC, the diet intervention alone significantly increased eNOS; when interventions of aerobic exercise but not diet control (MHE) were applied, they significantly decreased ox-LDL, MCP-1 and PAI-1 (P＜0.01); the applied interventions of both aerobic exercise and diet control (MRE) decreased ox-LDL, MCP-1 and PAI-1 and significantly decreased eNOS (P＜0.01). The MRE compared to MHE exhibited significant changes in MCP-1 and eNOS (P＜0.01). The mRNA levels of the processing markers of OS in the myocardium. Compared with C, the MS rats had significant increases in the chemotactic factor MPC-1 (P＜0.05) and the adhesion factor PAI-1 (P＜0.01), which indicated that MS rats exhibited enhanced OS. Moreover, the MS rats had an increased antioxidant marker of eNOS, which was not significant, and the regulatory factor of PPARα decreased (P＜0.01). Compared to MHC, the MRC rats exhibited decreased MPC-1 (P＞0.05) and PAI-1 (P＜0.05) and increased eNOS (P＜0.01) and PPARα (P＞0.05); moreover, the MHE and MRE rats decreased more in MPC-1 and PAI-1 (P＜0.01) with increased eNOS and PPARα (P＜0.01). Compared to MHE, the MRE rats had a further decrease in MPC-1 (P＜0.01) and PAI-1 (P＞0.05) with increased eNOS (P＜0.05) and PPARα (P＞0.05). Conclusions OS increased in MS rats. Moreover, aerobic exercise and alimentary control could decrease OS to reduce the damage in MS rats. The OS regulatory factor PPARα, which could mediate the expression of OS-related genes, such as MCP-1, PAI-1, and eNOS in cardiovascular tissues, was only enhanced by aerobic exercise and not by diet control.

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