Project description:We assessed vastus lateralis muscle gene expression levels of 12 women with the metabolic syndrome before and after a 6 month exercise training program RNA was isolated from a vastus lateralis muscle biopsy of 6 women with the metabolic syndrome before and after a 6 month guided endurance exercise training program
Project description:Changes and plasticity in both gene expression and protein signaling in skeletal muscle is considered to be a major cause of metabolic syndrome, while it has been shown that mild exercise training at lactate threshold (LT) intensity is a safe and effective for prevention of metabolic syndrome. To elucidate the molecular mechanisms related to the beneficial effects of LT training for 60 min/day for 5 days/wk for 12 wk, we performed serial analysis of gene expression (SAGE) to examine global mRNA expression in human skeletal muscle. Approximately 57000 SAGE tags were analyzed for before training, as well as 5 days, 6 and 12 wk after the training. The LT training has coordinately induced many genes involved in mitochondrial energy metabolism, fat oxidation, glycolysis and creatine metabolism. Another molecular feature associated with this mild exercise regimen has been an induction of many genes encoding for potent antioxidant enzymes and molecular chaperons. Furthermore, the training modulated the expression levels of 233 novel transcripts. Thus, the current study reveals that LT exercise has favorably altered gene expression in human skeletal muscle to the prevention of metabolic syndrome. Keywords: transcriptome, serial analysis of gene expression, metabolic syndrome, exercise training, lactate threshold
Project description:We assessed vastus lateralis muscle gene expression levels of 6 women with the metabolic syndrome before and after a 6 month exercise training program
Project description:We assessed vastus lateralis muscle gene expression levels of 12 women with the metabolic syndrome before and after a 6 month exercise training program
Project description:Low aerobic exercise capacity is a risk factor for diabetes and strong predictor of mortality; yet some individuals are exercise resistant, and unable to improve exercise capacity through exercise training. To test the hypothesis that resistance to aerobic exercise training underlies metabolic disease-risk, we used selective breeding for 15 generation to develop rat models of low- and high-aerobic response to training. Before exercise training, rats selected as low- and high-responders had similar exercise capacities. However, after 8-wks of treadmill training low-responders failed to improve their exercise capacity, while high-responders improved by 54%. Remarkably, low-responders to aerobic training exhibited pronounced metabolic dysfunction characterized by insulin resistance and increased adiposity, demonstrating that the exercise resistant phenotype segregates with disease risk. Low-responders had impaired exercise-induced angiogenes0is in muscle; however, mitochondrial capacity was intact and increased normally with exercise training, demonstrating that mitochondria are not limiting for aerobic adaptation or responsible for metabolic dysfunction in low-responders. Low-responders had increased stress/inflammatory signaling and altered TGFβ signaling, characterized by hyperphosphorylation of a novel exercise-regulated phosphorylation site on SMAD2. Using this powerful biological model system we have discovered key pathways for low exercise training response that may represent novel targets for the treatment of metabolic disease.
Project description:ATMs, which can constitute up to 50% of the cells in adipose tissue of obese mice 5, play a pivotal role in both metabolic and immune regulation of adipose tissue. This is particularly evident in both healthy states and in conditions associated with metabolic syndrome. To delve into the precise mechanisms of the ATMs in response to exercise, we utilized exercise-induced primary ATMs and miRNAs microarray to investigate the effects of an 8-week aerobic exercise training on ATMs. Following the exercise regimen, ATMs were sorted using flow cytometer and subsequently analyzed through bioinformatics analysis to identify changes in miRNA expression.
Project description:Skeletal muscle adapts to exercise training of various modes, intensities and durations with a programmed gene expression response. This study dissects the independent and combined effects of exercise mode, intensity and duration to identify which exercise has the most positive effects on skeletal muscle health. Full details on exercise groups can be found in: Kraus et al Med Sci Sports Exerc. 2001 Oct;33(10):1774-84 and Bateman et al Am J Cardiol. 2011 Sep 15;108(6):838-44. This study uses a middle aged group of subjects that have 3+ markers of metabolic syndrome. One group remains an inactive control, while 5 groups undergo 9 mo supervised exercise training. Exercise groups are as follows: Inactive control (group B); Mild aerobic exercise - low amount/mod intensity (group A); Moderate aerobic exercise - low amt/vig intensity (group D); High aerobic exercise - high amt/vig intensity (group C); resistance training only (group F); and mod aerobic + resistance training (group E). Each group has 10 subjects (5 men and 5 women), however 3 subjects failed array QC, leaving 8 subjects in group E and 9 subjects in group F. Data were all analyzed pre to post training in a RM ANCOVA, covaried for age and sex or regression to determine genotype/phenotype interactions.
Project description:Low aerobic exercise capacity is a risk factor for diabetes and strong predictor of mortality; yet some individuals are exercise resistant, and unable to improve exercise capacity through exercise training. To test the hypothesis that resistance to aerobic exercise training underlies metabolic disease-risk, we used selective breeding for 15 generation to develop rat models of low- and high-aerobic response to training. Before exercise training, rats selected as low- and high-responders had similar exercise capacities. However, after 8-wks of treadmill training low-responders failed to improve their exercise capacity, while high-responders improved by 54%. Remarkably, low-responders to aerobic training exhibited pronounced metabolic dysfunction characterized by insulin resistance and increased adiposity, demonstrating that the exercise resistant phenotype segregates with disease risk. Low-responders had impaired exercise-induced angiogenes0is in muscle; however, mitochondrial capacity was intact and increased normally with exercise training, demonstrating that mitochondria are not limiting for aerobic adaptation or responsible for metabolic dysfunction in low-responders. Low-responders had increased stress/inflammatory signaling and altered TGFM-NM-2 signaling, characterized by hyperphosphorylation of a novel exercise-regulated phosphorylation site on SMAD2. Using this powerful biological model system we have discovered key pathways for low exercise training response that may represent novel targets for the treatment of metabolic disease. Cardiac and skeletal muscle from 3 high and 3 low responder rats were examined for differential miRNA expression using Exiqon microarrays