Mitigation of chronic glucotoxicity-mediated skeletal muscle atrophy by arachidonic acid
Copyright © 2023 Elsevier Inc. All rights reserved..
Toxicity caused by chronic hyperglycemia is a significant factor affecting skeletal muscle myogenesis, resulting in diabetic myopathy. Chronic and persistent hyperglycemia causes activation of the atrophy-related pathways in the skeletal muscles, which eventually results in inflammation and muscle degeneration. To counteract this process, various bioactive compound has been studied for their reversal or hypertrophic effect. In this study, we explored the molecular mechanisms associated with reversing glucotoxicity's effect in C2C12 cells by arachidonic acid (AA). We found a substantial increase in the pro-inflammatory cytokines and ROS production in hyperglycemic conditions, mitigated by AA supplementation. We found that AA supplementation restored protein synthesis that was downregulated under glucotoxicity conditions. AA enhanced myogenesis by suppressing high glucose induced inflammation and ROS production and enhancing protein synthesis. These results imply that AA has cytoprotective actions against hyperglycemia-induced cytotoxicity.
Medienart: |
E-Artikel |
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Erscheinungsjahr: |
2023 |
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Erschienen: |
2023 |
Enthalten in: |
Zur Gesamtaufnahme - volume:333 |
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Enthalten in: |
Life sciences - 333(2023) vom: 15. Nov., Seite 122141 |
Sprache: |
Englisch |
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Beteiligte Personen: |
Mitra, Akash [VerfasserIn] |
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Links: |
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Themen: |
27YG812J1I |
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Anmerkungen: |
Date Completed 30.10.2023 Date Revised 30.10.2023 published: Print-Electronic Citation Status MEDLINE |
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doi: |
10.1016/j.lfs.2023.122141 |
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funding: |
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Förderinstitution / Projekttitel: |
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PPN (Katalog-ID): |
NLM36291334X |
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520 | |a Toxicity caused by chronic hyperglycemia is a significant factor affecting skeletal muscle myogenesis, resulting in diabetic myopathy. Chronic and persistent hyperglycemia causes activation of the atrophy-related pathways in the skeletal muscles, which eventually results in inflammation and muscle degeneration. To counteract this process, various bioactive compound has been studied for their reversal or hypertrophic effect. In this study, we explored the molecular mechanisms associated with reversing glucotoxicity's effect in C2C12 cells by arachidonic acid (AA). We found a substantial increase in the pro-inflammatory cytokines and ROS production in hyperglycemic conditions, mitigated by AA supplementation. We found that AA supplementation restored protein synthesis that was downregulated under glucotoxicity conditions. AA enhanced myogenesis by suppressing high glucose induced inflammation and ROS production and enhancing protein synthesis. These results imply that AA has cytoprotective actions against hyperglycemia-induced cytotoxicity | ||
650 | 4 | |a Journal Article | |
650 | 4 | |a Arachidonic acid | |
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700 | 1 | |a Das, Undurti N |e verfasserin |4 aut | |
700 | 1 | |a Shenoy P, Sudheer |e verfasserin |4 aut | |
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