Methionine sulfoxide reductase A affects insulin resistance by protecting insulin receptorfunction

Styskal, JennaLynn; Nwagwu, Florence A.; Watkins, Yvonne N.; Liang, Hanyu; Richardson, Arlan; Musi, Nicolas; Salmon, Adam B.

doi:10.1016/j.freeradbiomed.2012.10.544

Cited by 34 publications

(38 citation statements)

References 49 publications

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“…The modulation of antioxidant enzymes improves or aggravates insulin resistance by the high-fat diet via affecting the oxidative stress. Increased oxidative stress with deletion of antioxidant enzymes, such as methionine sulfoxide A, aggravates high-fat diet-induced insulin resistance (37). The overexpression of SOD2 ameliorates high-fat diet-induced insulin resistance in rat skeletal muscle (23).…”

Section: Discussionmentioning

confidence: 99%

Deficiency of Clusterin Exacerbates High-Fat Diet-Induced Insulin Resistance in Male Mice

Kwon

Heo

et al. 2014

Endocrinology

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The present study examined the role of clusterin in insulin resistance in high fat-fed wild-type and clusterin knockout (KO) mice. The plasma levels of glucose and C-peptide and islet size were increased in clusterin KO mice after an 8-week high-fat diet. In an ip glucose tolerance test, the area under the curve for glucose was not different, whereas the area under the curve for insulin was higher in clusterin KO mice. In a hyperinsulinemic-euglycemic clamp, the clamp insulin levels were higher in clusterin KO mice after the high-fat diet. After adjusting for the clamp insulin levels, the glucose infusion rate, suppression of hepatic glucose production, and glucose uptake were lower in clusterin KO mice in the high fat-fed group. The plasma levels of clusterin and clusterin mRNA levels in the skeletal muscle and liver were increased by the high-fat diet. The mRNA levels of the antioxidant enzymes were lower, and the mRNA levels of nicotinamide adenine dinucleotide phosphate oxidase (NOX) 1 and cytokines and protein carbonylation were higher in the skeletal muscle and liver in clusterin KO mice after the high-fat diet. Palmitate-induced gene expressions of NOX1 and cytokines were higher in the primary cultured hepatocytes of clusterin KO mice compared with the wild-type mice. Clusterin inhibited the gene expression and reactive oxygen species generation by palmitate in the hepatocytes and C2C12. AKT phosphorylation by insulin was reduced in the hepatocytes of clusterin KO mice. These results suggest that clusterin plays a protective role against high-fat diet-induced insulin resistance through the suppression of oxidative stress and inflammation.

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Section: Discussionmentioning

confidence: 99%

Deficiency of Clusterin Exacerbates High-Fat Diet-Induced Insulin Resistance in Male Mice

Kwon

Heo

et al. 2014

Endocrinology

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“…Increased levels of fatty acids induce oxidative stress, which leads to attenuated insulin-stimulated signaling pathways and insulin resistance (3). Reduced oxidative stress by overexpression of antioxidant enzyme in high fat-fed mice improves insulin resistance in mice (4), and a deletion of antioxidant enzymes in high fat-fed mice aggravates insulin resistance in mice (5).…”

Section: Introductionmentioning

confidence: 99%

Hemin Improves Insulin Sensitivity in Skeletal Muscle in High Fat–Fed Mice

Kwon

Kim

et al. 2014

J Pharmacol Sci

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Abstract. The present study examined whether hemin could prevent the development of high-fat diet-induced insulin resistance in the liver and skeletal muscle using a hyperinsulinemic-euglycemic clamp. A four-week high-fat feeding to mice increased the body weight, fat mass, and plasma levels of insulin and lipid, which were reduced by hemin. High-fat diet reduced whole body glucose uptake, which were increased by hemin. Insulin-stimulated hepatic glucose production (HGP) was increased by high-fat diet, but hemin had no significant effect on HGP. Skeletal muscle glucose uptake was reduced by high-fat diet, and hemin normalized the glucose uptake. High-fat diet increased triglyceride levels and mRNA levels of lipogenic enzymes, and decreased mRNA levels of enzymes involved in lipid b-oxidation, which was reversed by hemin. Phosphorylated AMPactivated protein kinase levels were increased in the skeletal muscle of high fat-fed hemin-injected mice. High-fat diet reduced mRNA levels of antioxidant enzymes and increased mRNA levels of inflammatory cytokines and nitrotyrosine levels, which was normalized by hemin in the skeletal muscle. However, hemin had no significant effect on these factors in the liver. These results suggest that hemin prevents the development of high-fat diet-induced insulin resistance by increased insulin sensitivity in the skeletal muscle.

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“…Several groups, including our own, have shown that obesity and high fat feeding are also associated with increased levels of oxidative stress and oxidative damage (6, 7, 12, 20, 21). In this study, we confirmed that high fat feeding is associated with increased levels of oxidative stress in multiple tissues.…”

Section: Resultsmentioning

confidence: 86%

Obesity-induced oxidative stress, accelerated functional decline with age and increased mortality in mice

Zhang

Fischer

Soto

et al. 2015

Archives of Biochemistry and Biophysics

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Obesity is a serious chronic disease that increases the risk of numerous co-morbidities including metabolic syndrome, cardiovascular disease and cancer as well as increases risk of mortality leading some to suggest this represents accelerated aging. Obesity is associated with significant increases in oxidative stress in vivo and, despite the well-explored relationship between oxidative stress and aging, the role this plays in the increased mortality of obese subjects remains an unanswered question. Here, we addressed this by undertaking a comprehensive, longitudinal study of a group of high fat-fed obese mice and assessed both their changes in oxidative stress and in their performance in physiological assays known to decline with aging. In female C57BL/6J mice fed a high-fat diet starting in adulthood, mortality was significantly increased in high fat-fed mice as was oxidative damage in vivo. High fat-feeding significantly accelerated the decline in performance in several assays, including activity, gait, and rotarod. However, we also found that obesity had little effect on other markers and actually improved performance in grip strength, a marker of muscular function. Together, this first comprehensive assessment of longitudinal functional changes in high fat-fed mice suggests that obesity may induce segmental acceleration of some of the aging process.

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Methionine sulfoxide reductase A affects insulin resistance by protecting insulin receptorfunction

Cited by 34 publications

References 49 publications

Deficiency of Clusterin Exacerbates High-Fat Diet-Induced Insulin Resistance in Male Mice

Deficiency of Clusterin Exacerbates High-Fat Diet-Induced Insulin Resistance in Male Mice

Hemin Improves Insulin Sensitivity in Skeletal Muscle in High Fat–Fed Mice

Obesity-induced oxidative stress, accelerated functional decline with age and increased mortality in mice

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