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ABSTRACT:
PROVIDER: PRJNA1214556 | ENA |
REPOSITORIES: ENA
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Project description:Microbiome research related to muscle strength improvement
| PRJEB85118 | ENA
Project description:The loss of muscle size, strength and quality with ageing, is a major determinant of morbidity and mortality in the elderly. The regulatory pathways that impact on the muscle phenotype include the translational regulation maintained by microRNAs (miRNA). Yet the miRNAs that are expressed in human skeletal muscle and whose expression levels correlate to muscle size, strength and quality are unknown. Here we used next-generation sequencing to characterise the expression profile of miRNAs in the m. vastus lateralis obtained by biopsy from middle-aged males (n=48; 50.0±4.3 years). Isokinetic strength testing and mid-thigh computed tomography was undertaken for muscle phenotype analysis. miR-486-5p accounted for 21% of the total miR sequence reads, with miR-10b-5p, miR-133a-3p, and miR-22-3p accounting for a further 15%, 12% and 10% respectively. Isokinetic knee extension strength and muscle cross-sectional area were positively correlated with miR-100-5p, miR-99b-5p and miR-191-5p expression. Whilst muscle attenuation, reflective of myofiber lipid content was negatively correlated to let-7f-5p, miR-30d-5p and miR-125b-5p expression. In-silico analysis implicates miRNAs related to strength and muscle size in the regulation of mammalian target of rapamycin, whist miRNAs related to muscle attenuation may have potential roles controlling the transforming growth factor- β/SMAD3 pathway which regulated fibrosis, adipogenesis and lipid accumulation.
2018-01-10 | GSE103635 | GEO
Project description:<p>The NHGRI Next Generation Mendelian Genetics project uses exome resequencing to identify variants in unsolved Mendelian diseases.</p> <p>Samples were collected from a single, multi-generational family with the same phenotype of exaggerated muscular development (muscular hypertrophy) and strength characterized by reduced fat pad thickness under the skin. All family members deny "body building" activities, and are so far negative for known gene mutation that have been identified as associated with excessive muscle development. All family members have examples of demonstrating extraordinary strength occurring both in childhood and old age. No negative associated phenotype traits with the muscle hypertrophy phenotype have been identified.</p>
| phs000541 | dbGaP
Project description:Both circulating endogenous testosterone and muscle AR protein content are positively associated with muscle mass and strength in males, but there is no such evidence in females. Here, we tested whether circulating testosterone levels were associated with muscle mass, function, transcriptome or the muscle anabolic response to resistance training in pre-menopausal females.
2025-05-17 | GSE267512 | GEO
Project description:This experiment was conducted to identify the mitochondrial protein changes in the presence and absence of LONP1 in skeletal muscle. The following abstract from the submitted manuscript describes the major findings of this work.Disuse-associated loss of muscle LONP1 impairs mitochondrial quality and causes reduced skeletal muscle mass and strength. Zhisheng Xu, Tingting Fu, Qiqi Guo, Danxia Zhou, Wanping Sun, Zheng Zhou, Lin Liu, Liwei Xiao, Yujing Yin, Yuhuan Jia, Xin Pan, Lei Fang, Min-sheng Zhu, Wenyong Fei, Bin Lu and Zhenji Gan. Mitochondrial proteolysis is an evolutionarily conserved quality control mechanism to maintain proper mitochondrial integrity and function. However, the physiological relevance of stress-induced impaired mitochondrial protein quality remains unclear. Here, we demonstrate that LONP1, a major mitochondrial protease resides in the matrix, plays a critical role in controlling mitochondrial quality as well as skeletal muscle mass and strength in response to muscle disuse. In humans and mice, disuse-related muscle loss is associated with decreased mitochondrial LONP1 protein. Skeletal muscle-specific ablation of LONP1 in mice resulted in impaired mitochondrial protein turnover, leading to mitochondrial dysfunction. This caused reduced muscle fiber size and strength. Mechanistically, aberrant accumulation of mitochondrial-retained protein in muscle upon loss of LONP1 induces the activation of autophagy-lysosome degradation program of muscle loss. Overexpressing a mitochondrial-retained mutant ornithine transcarbamylase (ΔOTC), a known protein degraded by LONP1, in skeletal muscle induces mitochondrial dysfunction, autophagy activation, and cause muscle loss and weakness. Thus, these findings reveal a pivotal role of LONP1-dependent mitochondrial protein quality-control in safeguarding mitochondrial function and preserving skeletal muscle mass and strength, and unravel an intriguing link between mitochondrial protein quality and muscle mass maintenance during muscle disuse.
2022-01-05 | PXD029722 | Pride
Project description:We previously reported that skeletal muscle adaptation to regular exercise requires a healthy gut microbiome, contributing to growing evidence that some exercise benefits are mediated by microbiome-derived metabolites. Here, to identify such exercise-associated microbial metabolites, we transfer cecal contents from exercise-trained donor mice into exercise-naïve recipient mice undergoing unilateral hindlimb immobilization. Recipients of cecal material from exercise-trained donors exhibit less muscle atrophy compared with those receiving transfers from sedentary donors. Untargeted metabolomics reveal metabolites enriched in cecal content, serum, and muscle of recipients from exercise-trained donors, consistent with microbial origin. Oral administration of two such metabolites (pipecolic acid and succinate) attenuates muscle atrophy and preserves muscle function in exercise-naïve mice, potentially by enhancing cellular energy status and translational capacity. These findings further define the gut microbiome-skeletal muscle axis and provide evidence that exercise-associated microbial metabolites serve as a novel class of exercise mimetics for treating conditions responsive to physical activity.
2026-05-27 | PXD077599 | Pride
Project description:<p>The NHGRI Next Generation Mendelian Genetics project uses exome resequencing to identify variants in unsolved Mendelian diseases.</p> <p>Samples were collected from a single, multi-generational family with the same phenotype of exaggerated muscular development (muscular hypertrophy) and strength characterized by reduced fat pad thickness under the skin. All family members deny "body building" activities, and are so far negative for known gene mutation that have been identified as associated with excessive muscle development. All family members have examples of demonstrating extraordinary strength occurring both in childhood and old age. No negative associated phenotype traits with the muscle hypertrophy phenotype have been identified.</p>
| phs000541.v1.p1 | EGA
Project description:We explore whether a low-energy diet intervention for Metabolic dysfunction-associated steatohepatitis (MASH) improves liver disease by means of modulating the gut microbiome. 16 individuals were given a low-energy diet (880 kcal, consisting of bars, soups, and shakes) for 12 weeks, followed by a stepped re-introduction to whole for an additional 12 weeks. Stool samples were obtained at 0, 12, and 24 weeks for microbiome analysis. Fecal microbiome were measured using 16S rRNA gene sequencing. Positive control (Zymo DNA standard D6305) and negative control (PBS extraction) were included in the sequencing. We found that low-energy diet improved MASH disease without lasting alterations to the gut microbiome.
2024-12-31 | E-MTAB-14061 | biostudies-arrayexpress
Project description:Background: Primary hyperparathyroidism (pHPT) is a common endocrine disorder leading to hypercalcemia and skeletal muscle dysfunction. Muscle weakness is associated with increased risk of morbidity and mortality but is overlooked in surgical guidelines for parathyroidectomy. While parathyroidectomy is the only curative treatment, its effects on skeletal muscle strength and molecular remodelling remain underexplored. Methods: We conducted a prospective observational cohort study involving 21 postmenopausal women with pHPT, of whom 15 completed the full protocol. Clinical assessments, magnetic resonance imaging (MRI), and skeletal muscle biopsies were performed before and three months post-parathyroidectomy. Muscle strength was evaluated using the timed stand test (TST) and isokinetic dynamometry, while RNA sequencing characterized transcriptomic changes in muscle biopsies. Findings: Parathyroidectomy normalized calcium and PTH levels, accompanied by significant improvements in muscle strength and composition. MRI revealed an increase in muscle volume and a reduction in fat fraction, without changes in physical activity levels. Transcriptomic analysis identified 981 differentially expressed genes post-surgery, enriched in pathways related to extracellular matrix remodelling, angiogenesis, and mitochondrial metabolism. Notably, transcriptional changes mirrored exercise-induced adaptations.
2026-01-28 | GSE283368 | GEO