Early potential effects of resveratrol supplementation on skeletal muscle adaptation involved in exercise-induced weight loss in obese mice
2
조회
0
다운로드
2
인용
0
참고문헌
키워드
초록
Exercise and resveratrol supplementation exhibit anti-obesity functions in the long term but have not been fully investigated yet in terms of their early potential effectiveness. Mice fed with high-fat diet were categorized into control (Cont), exercise (Ex), resveratrol supplementation (Res), and exercise combined with resveratrol supplementation (Ex + Res) groups. In the four-week period of weight loss, exercise combined with resveratrol supplementation exerted no additional effects on body weight loss but significantly improved whole-body glucose and lipid homeostasis. The combined treatment significantly decreased intrahepatic lipid content but did not affect intramyocellular lipid content. Moreover, the treatment significantly increased the contents of mtDNA and cytochrome c, the expression levels of peroxisome proliferator-activated receptor gamma coactivator-1 alpha and its downstream transcription factors, and the activities of ATPase and citrate synthase. However, exercise, resveratrol, and their combination did not promote myofiber specification toward slow-twitch type. The effects of exercise combined with resveratrol supplementation on weight loss could be partly due to enhanced mitochondrial biogenesis and not to fiber-type shift in skeletal muscle tissues.
Abstract
Exercise and resveratrol supplementation exhibit anti-obesity functions in the long term but have not been fully investigated yet in terms of their early potential effectiveness. Mice fed with high-fat diet were categorized into control (Cont), exercise (Ex), resveratrol supplementation (Res), and exercise combined with resveratrol supplementation (Ex + Res) groups. In the four-week period of weight loss, exercise combined with resveratrol supplementation exerted no additional effects on body weight loss but significantly improved whole-body glucose and lipid homeostasis. The combined treatment significantly decreased intrahepatic lipid content but did not affect intramyocellular lipid content. Moreover, the treatment significantly increased the contents of mtDNA and cytochrome c, the expression levels of peroxisome proliferator-activated receptor gamma coactivator-1 alpha and its downstream transcription factors, and the activities of ATPase and citrate synthase. However, exercise, resveratrol, and their combination did not promote myofiber specification toward slow-twitch type. The effects of exercise combined with resveratrol supplementation on weight loss could be partly due to enhanced mitochondrial biogenesis and not to fiber-type shift in skeletal muscle tissues.
참고문헌 (25)
- Chin SH, "Physical activity and obesity: what we know and what we need to know", Obes Rev, 17, pp.1226~1244 (2016)[DOI]
- Normandin E, "Effect of Resistance Training and Caloric Restriction on the Metabolic Syndrome", Med Sci Sports Exerc, 49, pp.413~419 (2017)
- Timmers S, "Calorie restriction-like effects of 30 days of resveratrol supplementation on energy metabolism and metabolic profile in obese humans", Cell Metab, 14, pp.612~622 (2011)[DOI]
- Haohao Z, "Resveratrol improves high-fat diet induced insulin resistance by rebalancing subsarcolemmal mitochondrial oxidation and antioxidantion", J Physiol Biochem, 71, pp.121~131 (2015)[DOI]
- Sparks LM, "A high-fat diet coordinately downregulates genes required for mitochondrial oxidative phosphorylation in skeletal muscle", Diabetes, 54, pp.1926~1933 (2005)[DOI]
- Civitarese AE, "Role of adiponectin in human skeletal muscle biogenesis", Cell Metab, 4, pp.75~87 (2006)[DOI]
- Mootha VK, "PGC-1alpha-responsive genes involved in oxidative phosphorylation are coordinately downregulated in human diabetes", Nat Genet, 34, pp.267~273 (2003)[DOI]
- Heilbronn LK, "Markers of mitochondrial biogenesis and metabolism are lower in overweight and obese insulin-resistant subjects", J Clin Endocrinol Metab, 92, pp.1467~1473 (2007)[DOI]
- Bonnard C, "Mitochondrial dysfunction results from oxidative stress in skeletal muscle of diet-induced insulin resistant mice", J Clin Invest, 118, pp.789~800 (2008)
- Benton CR, "PGC-1alphamediated regulation of gene expression and metabolism: implications for nutrition and exercise prescriptions", Appl Physiol Nutr Metab, 33, pp.843~862 (2008)[DOI]
- Despres JP, "Abdominal obesity and the metabolic syndrome: contribution to global cardiometabolic risk", Arterioscler Thromb Vasc Biol, 28, pp.1039~1049 (2008)[DOI]
- Brouwers B, "Effects of exercise training on intrahepatic lipid content in humans", Diabetologia, 59, pp.2068~2079 (2016)[DOI]
- Ahn J, "Dietary resveratrol alters lipid metabolism-related gene expression of mice on an atherogenic diet", J Hepatol, 9, pp.1019~1028 (2008)
- Savage DB, "Disordered lipid metabolism and the pathogenesis of insulin resistance", Physiol Rev, 87, pp.507~520 (2007)[DOI]
- Helge JW, "Effect of training on muscle triacylglycerol and structural lipids: a relation to insulin sensitivity", Diabetes, 52, pp.1881~1887 (2003)[DOI]
- Goodpaster BH, "Skeletal muscle lipid content and insulin resistance: evidence for a paradox in endurance-trained athletes", J Clin Endocrinol Metab, 86, pp.5755~5761 (2001)[DOI]
- Boushel R, "Patients with type 2 diabetes have normal mitochondrial function in skeletal muscle", Diabetologia, 50, pp.790~796 (2007)[DOI]
- Holloway GP, "Skeletal muscle mitochondrial FAT", CD36 content and palmitate oxidation are not decreased in obese women, 2007, pp.292, 1782~1789
- Wu Z, "Mechanisms controlling mitochondrial biogenesis and respiration through the thermogenic coactivator PGC-1", Cell, 98, pp.115~124 (1999)[DOI]
- Ji LL, "Role of PGC-<TEX>$1{\alpha}$<", TEX> in sarcopenia: etiology and potential intervention-a mini-review, 2015, pp.61, 139~148
- Atherton PJ, "Selective activation of AMPK-PGC-1alpha or PKB-TSC2-mTOR signaling can explain specific adaptive responses to endurance or resistance training-like electrical muscle stimulation", FASEB J, 19, pp.786~788 (2005)[DOI]
- Valero T, "Mitochondrial biogenesis: pharmacological approaches", Curr Pharm Des, 20, pp.5507~5509 (2014)[DOI]
- Lin J, "Transcriptional co-activator PGC-1 alpha drives the formation of slow-twitch muscle fibres", Nature, 418, pp.797~801 (2002)[DOI]
- Sun J, "Early Mitochondrial Adaptations in Skeletal Muscle to Obesity and Obesity Resistance Differentially Regulated by High-Fat Diet", Exp Clin Endocrinol Diabetes, 125, pp.538~546 (2017)[DOI]
- O'Neill BT, "A conserved role for phosphatidylinositol 3-kinase but not Akt signaling in mitochondrial adaptations that accompany physiological cardiac hypertrophy", Cell Metab, 6, pp.294~306 (2007)[DOI]
