title: Vitamin E and vitamin C do not reduce insulin sensitivity but inhibit mitochondrial protein expression in exercising obese rats.
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.
authors.affiliation: USDA-ARS Grand Forks Human Nutrition Research Center, 2420 2nd Avenue North, Grand Forks, ND 58201, USA.
authors.forename: Matthew J
authors.initials: MJ
authors.lastname: Picklo
authors.forename: John P
authors.initials: JP
authors.lastname: Thyfault
mesh_terms: D000273:Adipose Tissue / Q000187:drug effects / Q000378:metabolism; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D001205:Ascorbic Acid / Q000494:pharmacology*; D002784:Cholesterol / Q000097:blood; D004272:DNA, Mitochondrial / Q000378:metabolism; D023381:Endpoint Determination; D005951:Glucose Tolerance Test; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D008297:Male; D024101:Mitochondrial Proteins / Q000235:genetics / Q000378:metabolism*; D018482:Muscle, Skeletal / Q000187:drug effects / Q000378:metabolism; D061087:NADP Transhydrogenase, AB-Specific / Q000235:genetics / Q000378:metabolism*; D009765:Obesity / Q000378:metabolism*; D010805:Physical Conditioning, Animal; D051381:Rats; D017207:Rats, Sprague-Dawley; D014280:Triglycerides / Q000097:blood; D014810:Vitamin E / Q000494:pharmacology*
chemical_list: D000975:Antioxidants; D004272:DNA, Mitochondrial; D007328:Insulin; D024101:Mitochondrial Proteins; D014280:Triglycerides; D014810:Vitamin E; D002784:Cholesterol; D061087:NADP Transhydrogenase, AB-Specific; C556047:Nnt protein, rat; D001205:Ascorbic Acid
keywords: acide ascorbique; antioxidants; antioxydants; ascorbic acid; biogenesis; biogenèse; glucose tolerance; insulin resistance; insulinorésistance; mitochondria; mitochondrie; tocopherol; tocophérol; tolérance au glucose