scholarly journals The Lipid Peroxidation By-Product 4-Hydroxy-2-Nonenal (4-HNE) Induces Insulin Resistance in Skeletal Muscle through Both Carbonyl and Oxidative Stress

Endocrinology ◽  
2012 ◽  
Vol 153 (5) ◽  
pp. 2099-2111 ◽  
Author(s):  
Nicolas J. Pillon ◽  
Marine L. Croze ◽  
Roxane E. Vella ◽  
Laurent Soulère ◽  
Michel Lagarde ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Lipid Peroxidation ◽  
And Oxidative Stress

scholarly journals Effect of L-Carnitine on Skeletal Muscle Lipids and Oxidative Stress in Rats Fed High-Fructose Diet

2007 ◽  
Vol 2007 ◽  
pp. 1-8 ◽  
Author(s):  
Panchamoorthy Rajasekar ◽  
Carani Venkatraman Anuradha
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Intraperitoneal Administration ◽  
Protein Carbonyls ◽  
Sensitivity Index ◽  
Rat Tissues ◽  
High Fructose Diet ◽  
High Fructose ◽  
And Oxidative Stress

There is evidence that high-fructose diet induces insulin resistance, alterations in lipid metabolism, and oxidative stress in rat tissues. The purpose of this study was to evaluate the effect of L-carnitine (CAR) on lipid accumulation and peroxidative damage in skeletal muscle of rats fed high-fructose diet. Fructose-fed animals (60 g/100 g diet) displayed decreased glucose/insulin (G/I) ratio and insulin sensitivity index (ISI0,120) indicating the development of insulin resistance. Rats showed alterations in the levels of triglycerides, free fatty acids, cholesterol, and phospholipids in skeletal muscle. The condition was associated with oxidative stress as evidenced by the accumulation of lipid peroxidation products, protein carbonyls, and aldehydes along with depletion of both enzymic and nonenzymic antioxidants. Simultaneous intraperitoneal administration of CAR (300 mg/kg/day) to fructose-fed rats alleviated the effects of fructose. These rats showed near-normal levels of the parameters studied. The effects of CAR in this model suggest that CAR supplementation may have some benefits in patients suffering from insulin resistance.

Skeletal muscle insulin resistance: role of inflammatory cytokines and reactive oxygen species

2008 ◽  
Vol 294 (3) ◽  
pp. R673-R680 ◽  
Author(s):  
Yongzhong Wei ◽  
Kemin Chen ◽  
Adam T. Whaley-Connell ◽  
Craig S. Stump ◽  
Jamal A. Ibdah ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Inflammatory Cytokines ◽  
Molecular Mechanisms ◽  
Low Grade ◽  
Muscle Insulin Resistance ◽  
Skeletal Muscle Insulin Resistance ◽  
Increased Risk ◽  
And Oxidative Stress

The cardiometabolic syndrome (CMS), with its increased risk for cardiovascular disease (CVD), nonalcoholic fatty liver disease (NAFLD), and chronic kidney disease (CKD), has become a growing worldwide health problem. Insulin resistance is a key factor for the development of the CMS and is strongly related to obesity, hyperlipidemia, hypertension, type 2 diabetes mellitus (T2DM), CKD, and NAFLD. Insulin resistance in skeletal muscle is particularly important since it is normally responsible for more than 75% of all insulin-mediated glucose disposal. However, the molecular mechanisms responsible for skeletal muscle insulin resistance remain poorly defined. Accumulating evidence indicates that low-grade chronic inflammation and oxidative stress play fundamental roles in the development of insulin resistance, and inflammatory cytokines likely contribute to the link between inflammation, oxidative stress, and skeletal muscle insulin resistance. Understanding the mechanisms by which skeletal muscle tissue develops resistance to insulin will provide attractive targets for interventions, which may ultimately curb this serious problem. This review is focused on the effects of inflammatory cytokines and oxidative stress on insulin signaling in skeletal muscle and consequent development of insulin resistance.

Time course of skeletal muscle loss and oxidative stress in rats with walker 256 solid tumor

2010 ◽  
Vol 42 (6) ◽  
pp. 950-958 ◽  
Author(s):  
Flávia A. Guarnier ◽  
Alessandra L. Cecchini ◽  
Andréia A. Suzukawa ◽  
Ana Leticia G.C. Maragno ◽  
Andréa N.C. Simão ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Solid Tumor ◽  
Time Course ◽  
Muscle Loss ◽  
Skeletal Muscle Loss ◽  
Walker 256 ◽  
And Oxidative Stress

Nose-only water-pipe smoking effects on airway resistance, inflammation, and oxidative stress in mice

2013 ◽  
Vol 115 (9) ◽  
pp. 1316-1323 ◽  
Author(s):  
Abderrahim Nemmar ◽  
Haider Raza ◽  
Priya Yuvaraju ◽  
Sumaya Beegam ◽  
Annie John ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Airway Resistance ◽  
Reduced Glutathione ◽  
Mechanistic Explanation ◽  
The United States ◽  
Forced Oscillation Technique ◽  
Water Pipe ◽  
Respiratory Effects ◽  
And Oxidative Stress

Water-pipe smoking (WPS) is a common practice in the Middle East and is now gaining popularity in Europe and the United States. However, there is a limited number of studies on the respiratory effects of WPS. More specifically, the underlying pulmonary pathophysiological mechanisms related to WPS exposure are not understood. Presently, we assessed the respiratory effects of nose-only exposure to mainstream WPS generated by commercially available honey flavored “moasel ” tobacco. The duration of the session was 30 min/day and 5 days/wk for 1 mo. Control mice were exposed to air only. Here, we measured in BALB/c mice the airway resistance using forced-oscillation technique. Lung inflammation was assessed histopathologically and by biochemical analysis of bronchoalveolar lavage (BAL) fluid, and oxidative stress was evaluated biochemically by measuring lipid peroxidation, reduced glutathione and several antioxidant enzymes. Pulmonary inflammation assessment showed an increase in neutrophil and lymphocyte numbers. Likewise, airway resistance was significantly increased in the WPS group compared with controls. Tumor necrosis factor α and interleukin 6 concentrations were significantly increased in BAL fluid. Lipid peroxidation in lung tissue was significantly increased whereas the level and activity of antioxidants including reduced glutathione, glutathione S transferase, and superoxide dismutase were all significantly decreased following WPS exposure, indicating the occurrence of oxidative stress. Moreover, carboxyhemoglobin levels were significantly increased in the WPS group. We conclude that 1-mo nose-only exposure to WPS significantly increased airway resistance, inflammation, and oxidative stress. Our results provide a mechanistic explanation for the limited clinical studies that reported the detrimental respiratory effects of WPS.

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