ArticleCellular and molecular life sciences : CMLS2022
Melatonin relieves hepatic lipid dysmetabolism caused by aging via modifying the secondary bile acid pattern of gut microbes.
Article in Cellular and molecular life sciences : CMLS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 51 citations in OpenAlex.
- Melatonin: Roles and Molecular Mechanisms in Metabolic Dysfunction-Associated Steatotic Liver Disease.Biomolecules · 2026Review
- Gut microbiota preserves bone mass through modulating the hyodeoxycholic acid-TGR5 axis.Gut microbes · 2025Article
- Adipocyte FMO3-derived TMAO induces WAT dysfunction and metabolic disorders by promoting inflammasome activation in ageing.Nature communications · 2025Article
- Cholecystectomy-related gut microbiota dysbiosis exacerbates colorectal tumorigenesis.Nature communications · 2025Article
- Differential roles of individual bile acid in physiology and disease.Pharmacological research · 2025Review
- Crosstalk Between Bile Acids and Intestinal Epithelium: Multidimensional Roles of Farnesoid X Receptor and Takeda G Protein Receptor 5.International journal of molecular sciences · 2025Review
- Tauroursodeoxycholic acid targets HSP90 to promote protein homeostasis and extends healthy lifespan.Science China. Life sciences · 2025Article
- Achieving healthy aging through gut microbiota-directed dietary intervention: Focusing on microbial biomarkers and host mechanisms.Journal of advanced research · 2025Review
- The Protective Effects of Melatonin on Hainan Black Goats Under Heat Stress: Understanding Its Actions and Mechanisms.Antioxidants (Basel, Switzerland) · 2025Article
- Protective Effects of Exogenous Melatonin Administration on White Fat Metabolism Disruption Induced by Aging and a High-Fat Diet in Mice.Antioxidants (Basel, Switzerland) · 2024Article
- Distinct signatures of gut microbiota and metabolites in primary biliary cholangitis with poor biochemical response after ursodeoxycholic acid treatment.Cell & bioscience · 2024Article
- Unveiling the oral-gut connection: chronic apical periodontitis accelerates atherosclerosis via gut microbiota dysbiosis and altered metabolites in apoEInternational journal of oral science · 2024Article
- The Therapeutic Trip of Melatonin Eye Drops: From the Ocular Surface to the Retina.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Multi-omics insights implicate the remodeling of the intestinal structure and microbiome in aging.Frontiers in genetics · 2024Article
- Matcha alleviates obesity by modulating gut microbiota and its metabolites.Current research in food science · 2024Article
- USP14 governs CYP2E1 to promote nonalcoholic fatty liver disease through deubiquitination and stabilization of HSP90AA1.Cell death & disease · 2023Article
- Review
- Mechanism of action and promising clinical application of melatonin from a dermatological perspective.Journal of translational autoimmunity · 2023Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
It has been reported that aging-generated gut microecosystem may promote host hepatic lipid dysmetabolism through shaping the pattern of secondary bile acids (BAs). Then as an oral drug, melatonin (Mel)-mediated beneficial efforts on the communication between gut microbiota and aging host are still not clearly. Here, we show that aging significantly shapes the pattern of gut microbiota and BAs, whereas Mel treatment reverses these phenotypes (P < 0.05), which is identified to depend on the existence of gut microbiota. Mechanistically, aging-triggered high-level expression of ileac farnesoid X receptor (FXR) is significantly decreased through Mel-mediated inhibition on Campylobacter jejuni (C. jejuni)-induced deconjugation of tauroursodeoxycholic acid (TUDCA) and glycoursodeoxycholic acid (GUDCA) (P < 0.05). The aging-induced high-level of serum taurine chenodeoxycholic acid (TCDCA) activate trimethylamine-N-oxide (TMAO)-triggered activating transcriptional factor 4 (ATF4) signaling via hepatic FXR, which further regulates hepatic BAs metabolism, whereas TUDCA inhibits aging-triggered high-level of hepatic ATF4. Overall, Mel reduces C. jejuni-mediated deconjugation of TUDCA to inhibit aging-triggered high-level expression of hepatic FXR, which further decreases hepatic TMAO production, to relieve hepatic lipid dysmetabolism.
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Registered trials
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