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Appl Physiol Nutr Metab. 2015 Apr;40(4):343-52. doi: 10.1139/apnm-2014-0302. Epub 2014 Dec 9.

Vitamin E and vitamin C do not reduce insulin sensitivity but inhibit mitochondrial protein expression in exercising obese rats.

Author information

1
USDA-ARS Grand Forks Human Nutrition Research Center, 2420 2nd Avenue North, Grand Forks, ND 58201, USA.

Abstract

Controversy exists as to whether supplementation with the antioxidants vitamin E and vitamin C blocks adaptation to exercise. Exercise is a first-line means to treat obesity and its complications. While diet-induced obesity alters mitochondrial function and induces insulin resistance (IR), no data exist as to whether supplementation with vitamin E and vitamin C modify responses to exercise in pre-existing obesity. We tested the hypothesis that dietary supplementation with vitamin E (0.4 g α-tocopherol acetate/kg) and vitamin C (0.5 g/kg) blocks exercise-induced improvements on IR and mitochondrial content in obese rats maintained on a high-fat (45% fat energy (en)) diet. Diet-induced obese, sedentary rats had a 2-fold higher homeostasis model assessment of insulin resistance and larger insulin area under the curve following glucose tolerances test than rats fed a low-fat (10% fat en) diet. Exercising (12 weeks at 5 times per week in a motorized wheel) of obese rats normalized IR indices, an effect not modified by vitamin E and vitamin C. Vitamin E and vitamin C supplementation with exercise elevated mtDNA content in adipose and skeletal muscle to a greater extent (20%) than exercise alone in a depot-specific manner. On the other hand, vitamin C and vitamin E decreased exercise-induced increases in mitochondrial protein content for complex I (40%) and nicotinamide nucleotide transhydrogenase (35%) in a muscle-dependent manner. These data indicate that vitamin E and vitamin C supplementation in obese rodents does not modify exercise-induced improvements in insulin sensitivity but that changes in mitochondrial biogenesis and mitochondrial protein expression may be modified by antioxidant supplementation.

KEYWORDS:

acide ascorbique; antioxidants; antioxydants; ascorbic acid; biogenesis; biogenèse; glucose tolerance; insulin resistance; insulinorésistance; mitochondria; mitochondrie; tocopherol; tocophérol; tolérance au glucose

PMID:
25761734
PMCID:
PMC4713234
DOI:
10.1139/apnm-2014-0302
[Indexed for MEDLINE]
Free PMC Article

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