Melatonin Mitigates Sarcopenic Obesity via Microbiota and Short-Chain Fatty Acids: Evidence From Epidemiologic and In Vivo Studies
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View abstract on PubMed
Summary
This summary is machine-generated.Melatonin (MLT) mitigates high-fat diet-induced sarcopenic obesity (SO) by regulating gut microbiota and increasing short-chain fatty acids (SCFAs). This suggests MLT as a potential therapeutic strategy for SO progression.
Area Of Science
- Metabolic disorders
- Gut microbiota
- Muscle physiology
Background
- Gut dysbiosis is linked to sarcopenic obesity (SO).
- Melatonin (MLT) influences gut microbiota and short-chain fatty acid (SCFA) production.
- The role of MLT in SO via gut microbiota and SCFAs requires elucidation.
Purpose Of The Study
- To investigate the effects and mechanisms of MLT on SO induced by a high-fat diet (HFD).
- To explore the association between MLT levels and SO parameters in patients.
- To determine MLT's impact on gut microbiota, SCFAs, and gut barrier integrity in an HFD-induced rat model.
Main Methods
- Case-control study in 31 patients to correlate serum MLT with SO parameters.
- HFD-induced rat model treated with MLT for 16 weeks.
- Analysis of gut microbiota (16S rRNA), SCFAs (GC-MS), and gut barrier proteins (Muc-2, tight junctions).
- Faecal microbiota transplantation and SCFA administration to confirm causality.
Main Results
- Lower serum MLT levels observed in SO patients, correlating with muscle mass and strength.
- MLT treatment in HFD rats ameliorated metabolic disorders, muscle atrophy, and improved muscle function.
- MLT modulated gut microbiota, increasing SCFA-producing bacteria and SCFAs, and restored gut barrier integrity.
- Faecal transfer from MLT-treated rats partially alleviated SO symptoms in recipients; SCFA treatment improved muscle parameters via AKT/mTOR/p70S6k pathway.
Conclusions
- MLT mitigates HFD-induced SO by regulating gut microbiota and promoting SCFA production.
- MLT demonstrates potential as a novel strategy for delaying SO progression.
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