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ARS Home » Plains Area » Grand Forks, North Dakota » Grand Forks Human Nutrition Research Center » Dietary Prevention of Obesity-related Disease Research » Research » Publications at this Location » Publication #307884
Title: Vitamin E and vitamin C do not reduce insulin sensitivity but inhibit mitochondrial protein expression in exercising obese rats

Author
item Picklo, Matthew
item THYFAULT, JOHN - University Of Missouri

Submitted to: Applied Physiology, Nutrition & Metabolism
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 12/9/2014
Publication Date: 4/1/2015
Publication URL: http://handle.nal.usda.gov/10113/60654
Citation: Picklo, M.J., Thyfault, J.P. 2015. Vitamin E and vitamin C do not reduce insulin sensitivity but inhibit mitochondrial protein expression in exercising obese rats. Applied Physiology, Nutrition & Metabolism. 40(4):343-352.

Interpretive Summary: Obesity, in combination with a lack of exercise, leads to dysfunction of the energy producing parts of the cells, the mitochondria, and induces insulin resistance, a problem facing over 75 million people in the United States alone. Exercise is a proven way of preventing or reversing these problems. Although many people take antioxidant supplements, some reports suggest that antioxidant supplements may block the insulin-improving and mitochondria-improving effects of exercise. In this study, obese rats were exercised with and without supplementation with the antioxidants vitamin E and vitamin C. Our results show that supplementation with vitamin E and vitamin C did not prevent nor add to the positive effects of exercise on insulin signaling. However, supplementation did block exercise-induced changes in muscle mitochondrial proteins. Our data suggest that supplementation with vitamin E and vitamin C does not provide added benefit to exercise.

Technical Abstract: Controversy exists as to whether supplementation with the antioxidants vitamin E (VE) and vitamin C (VC) blocks adaptation to exercise. Exercise is a first-line means to treat obesity and its complications. While diet-induced obesity alters mitochondrial (MT) function and induces insulin resistance (IR), no data exist as to whether supplementation with VE and VC modify responses to exercise in pre-existing obesity. We tested the hypothesis that dietary supplementation with VE (0.4 g alpha-tocopherol acetate/kg) and VC (0.5g/kg) blocks exercise-induced improvements on IR and MT content in obese rats maintained on a high-fat (45% fat energy) diet. Diet-induced obese, sedentary rats had a 2-fold higher HOMA-IR and insulin area under the curve following glucose tolerances test than rats fed a low-fat (10% fat en), eucaloric diet. Exercising (12 wks at five times per week in a motorized wheel) of obese rats normalized IR indices, an effect not modified by VE and VC. VE and VC supplementation with exercise elevated MT DNA content in adipose and skeletal muscle to a greater extent (20%) than exercise alone in a depot specific manner. On the other hand, VC and VE decreased exercise-induced increases in MT protein content for complex I (40%) and nicotinamide nucleotide transhydrogenase (35%) in a muscle-dependent manner. These data indicate that VE and VC supplementation in obese rodents does not modify exercise-induced improvements in insulin sensitivity but that changes in MT biogenesis and MT protein expression may be modified by antioxidant supplementation.