Brain protein lactylation after exercise training
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus Musculus
SUBMITTER: 
Li Zhang
PROVIDER: PXD053340 | iProX | Fri Jun 21 00:00:00 BST 2024
REPOSITORIES: iProX
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Project description:To explore the effects of moderate intensity exercise on protein of lactylation in mouse muscle tissue metabolism. The healthy adult mice running for 6 weeks as exercise model and sedentary mice as control were used to perform transcriptomic, proteomic, lactylation-proteomics, and metabolomics analysis. In addition, correlation analysis between transcriptome and proteome, and proteome and metabolome was conducted as well.
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Project description:Regular exercise improves health and prevents many chronic disorders such as obesity, cardiovascular and neurological diseases. Here, we hypothesized that skeletal muscle gene enhancers undergo epigenetic remodeling after exercise training and overlap with known disease variants from genome-wide association studies (GWAS). Overlapping exercise-remodeled enhancers with GWAS and cis-expression Quantitative Trait Loci data revealed enrichment with traits related to platelet function, cognitive traits and cardiovascular disease. We identify FBXW4 and PLEKHO2 as candidate genes regulated by variant-containing, exercise-responsive enhancers, and that are potentially involved in the distal modulation of brain function. Our results identify a list of genes differentially regulated after exercise training in humans, and which may cooperatively control brain function through the cardiovascular system.
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Project description:To explore the effects of moderate intensity exercise on protein of lactylation in mouse muscle tissue metabolism. The healthy adult mice running for 6 weeks as exercise model and sedentary mice as control were used to perform transcriptomic, proteomic, lactylation-proteomics, and metabolomics analysis. In addition, correlation analysis between transcriptome and proteome, and proteome and metabolome was conducted as well. In this study, 159 lactate sites of 78 proteins were identified to be differentically regulated by moderate intensity exercise. Enrichment analysis showed that lactated proteins Mtatp8, Atp5mg and Atp5po exhibited ATP hydrolysis activity. They are involved in biological processes such as mitochondrial transmembrane transport, and Mtatp8, Atp5mg and Atp5po participate in Oxidative phosphorylation and Thermogenesis pathways. The lactation levels of Mtatp8, Atp5mg and Atp5po proteins in exercise group were significantly decreased, while their protein levels were significantly increased. The combined analysis of proteomics and metabolomics showed that the Oxocarboxylic acid metabolism pathway and Sphingolipid signaling pathway had significant changes under the influence of moderate intensity exercise. Our results showed that moderate intensity exercise has a certain effect on the lactylation level of mice, possibly by reducing lactylation levels of Mtatp8, Atp5mg and Atp5po and increasing the expression of their protein levels, thereby regulating the Oxidative phosphorylation pathway and participating in energy metabolism. 2-Oxocarboxylic acid metabolism pathway and Sphingolipid signaling pathway need to be further explored.
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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
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