BAIBA in soleus from BAIBA-treated HFD-fed mice
Ontology highlight
ABSTRACT:
INSTRUMENT(S): Illumina HiSeq 1500, Illumina
ORGANISM(S): Mus musculus
SUBMITTER: Chew Weng Cheng
PROVIDER: E-MTAB-14747 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:The metabolite beta-aminoisobutyric acid (BAIBA) as an exercise-induced muscle-derived signal regulating adipose tissue metabolism during exercise. Here, we determine that BAIBA mimics aerobic exercise training effects on human skeletal myocytes.
2026-06-22 | E-MTAB-14746 | biostudies-arrayexpress
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Project description:Although skeletal muscle metabolism is a well-studied physiological process, little is known about how it is regulated at the transcriptional level. The myogenic transcription factor myogenin is required for skeletal muscle development during embryonic and fetal life, but myogeninâs role in adult skeletal muscle is unclear. We sought to determine myogeninâs function in adult muscle metabolism. A Myog conditional allele and Cre-ER transgene were used to delete Myog in adult mice. Mice were analyzed for exercise capacity by involuntary treadmill running. To assess oxidative and glycolytic metabolism, we monitored blood glucose and lactate levels and performed histochemical analysis on muscle fibers. Surprisingly, we found that Myog-deleted mice performed significantly better than controls in high- and low-intensity treadmill running. This enhanced exercise capacity was due to more efficient oxidative metabolism during low-intensity exercise and more efficient glycolytic metabolism during high-intensity exercise. Furthermore, Myog-deleted mice had an enhanced response to long-term voluntary exercise training on running wheels. We identified several candidate genes whose expression was altered in exercise-stressed muscle of mice lacking myogenin. The results suggest that myogenin plays a critical role as a high-level transcriptional regulator to control the energy balance between aerobic and anaerobic metabolism in adult skeletal muscle. We used microarrays to detail the global program of gene expression underlying enhanced exercise endurance associated with myog-deletion and long-term exercise training. Mouse gastrocnemius muscles were selected after 6 months of myog-deletion and exercise training for RNA extraction and hybridization on Affymetrix microarrays. We chose 3 wild type and 3 myog-deleted mice that best represented the average of each larger group that was tested during our mouse exercise studies.
2010-06-08 | E-GEOD-22046 | biostudies-arrayexpress
Project description:Purpose: Aerobic capacity is a strong predictor of cardiovascular mortality. To determine the relationship between inborn aerobic capacity and soleus gene expression we examined genome-wide gene expression in soleus muscle of rats artificially selected for high and low running capacity (HCR and LCR, respectively) over 16 generations. The artificial selection of LCR caused accumulation of risk factors of cardiovascular disease similar to the metabolic syndrome seen in man, whereas HCR had markedly better cardiac function. We also studied alterations in gene expression in response to exercise training in the two groups, since accumulating evidence indicates that exercise has profound beneficial effects on the metabolic syndrome. Methods: Soleus gene expression of both sedentary and exercise trained HCR and LCR was characterized by microarray- and gene ontology analysis. Results: Although HCR and LCR had an inborn 347% difference in running capacity, only three genes were found differentially expressed in the soleus muscle between the two groups. Up-regulation of the mitochondrial enzyme leucyl-transferRNA synthetase (LARS2) was found in the sedentary LCR. Increased expression of LARS2 has been associated with a mitochondrial DNA mutation linked to maternally inherited diabetes and mitochondrial dysfunction. In line with our findings, a growing body of evidence suggests that LCR have compromised mitochondrial function. After exercise training, 58 genes were altered in the soleus muscle of HCR, in contrast to only one in the LCR group. This suggests that animals born with different levels of fitness respond different to the same type of exercise training. Adaptations to exercise in HCR seemed to be associated with increased lipid metabolism and fatty acid elongation in the mitochondria. Also, genes associated with the peroxisomes, seemed to be central in the adaptation to exercise. Conclusion: The results indicate that (i) LCR might have mitochondrial dysfunction, which may be a contributing factor of the low inborn aerobic capacity, (ii) animals born with different levels of fitness respond different to the same exercise program. Keywords: aerobic capacity, metabolic syndrome, soleus muscle, gene expression, metabolism
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Project description:The aim of the project is to investigate whether endothelial-restricted augmentation of IGF-1 signaling is sufficient to suppress atherogenesis. We generated RNA-seq data from mice with endothelial-restricted over-expression of human wildtype IGF-1R (hIGFREO/ApoE-/-) or a signaling defective K1003R mutant human IGF-1R (mIGFREO/ApoE-/-).
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Project description:Purpose: Aerobic capacity is a strong predictor of cardiovascular mortality. To determine the relationship between inborn aerobic capacity and soleus gene expression we examined genome-wide gene expression in soleus muscle of rats artificially selected for high and low running capacity (HCR and LCR, respectively) over 16 generations. The artificial selection of LCR caused accumulation of risk factors of cardiovascular disease similar to the metabolic syndrome seen in man, whereas HCR had markedly better cardiac function. We also studied alterations in gene expression in response to exercise training in the two groups, since accumulating evidence indicates that exercise has profound beneficial effects on the metabolic syndrome. Methods:; Soleus gene expression of both sedentary and exercise trained HCR and LCR was characterized by microarray- and gene ontology analysis. Results: Although HCR and LCR had an inborn 347% difference in running capacity, only three genes were found differentially expressed in the soleus muscle between the two groups. Up-regulation of the mitochondrial enzyme leucyl-transferRNA synthetase (LARS2) was found in the sedentary LCR. Increased expression of LARS2 has been associated with a mitochondrial DNA mutation linked to maternally inherited diabetes and mitochondrial dysfunction. In line with our findings, a growing body of evidence suggests that LCR have compromised mitochondrial function. After exercise training, 58 genes were altered in the soleus muscle of HCR, in contrast to only one in the LCR group. This suggests that animals born with different levels of fitness respond different to the same type of exercise training. Adaptations to exercise in HCR seemed to be associated with increased lipid metabolism and fatty acid elongation in the mitochondria. Also, genes associated with the peroxisomes, seemed to be central in the adaptation to exercise. Conclusion: The results indicate that (i) LCR might have mitochondrial dysfunction, which may be a contributing factor of the low inborn aerobic capacity, (ii) animals born with different levels of fitness respond different to the same exercise program. Experiment Overall Design: There are 16 samples in this study.
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Project description:Endurance exercise training has been shown to decrease whole-body and skeletal muscle insulin resistance and increase glucose tolerance in conditions of both pre-diabetes and overt type 2 diabetes. However, the adaptive responses in skeletal muscle at the molecular and genetic level for these beneficial effects of exercise training have not been clearly established in an animal model of pre-diabetes. The present study identifies alterations in skeletal muscle gene expression that occur with exercise training in pre-diabetic, insulin-resistant obese Zucker (fa/fa) rats and insulin-sensitive lean Zucker (Fa/-) rats. Treadmill running for up to 4 weeks caused significant enhancements of glucose tolerance as assessed by the integrated area under the curve for glucose (AUCg) during an oral glucose tolerance test in both lean and obese animals. Using microarray analysis, a set of only 12 genes was identified as both significantly altered (>1.5-fold change relative to sedentary controls; p<0.05) and significantly correlated (p<0.05) with the AUCg. Two of these genes, peroxisome proliferator-activated receptor-g coactivator 1a (PGC-1a) and the z-isoform of protein kinase C (PKC-z), have known involvement in the regulation of skeletal muscle glucose transport. We confirmed that protein expression levels of PGC-1a and PKC-z were positively correlated with the mRNA expression levels for these two genes. Overall, this study has identified a limited number of genes in soleus muscle of lean and obese Zucker rats that are associated with decreased insulin resistance and increase glucose tolerance following endurance exercise training. These findings could guide the development of pharmaceutical M-^Sexercise mimeticsM-^T in the treatment of insulin-resistant, pre-diabetic or overtly type 2 diabetic individuals.
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