ArticleMolecular medicine (Cambridge, Mass.)2023
Swimming exercise ameliorates insulin resistance and nonalcoholic fatty liver by negatively regulating PPARγ transcriptional network in mice fed high fat diet.
Article in Molecular medicine (Cambridge, Mass.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- Metabolic dysfunction-associated steatotic liver disease: pathogenic mechanisms and exercise-induced molecular adaptations.Lipids in health and disease · 2026Review
- Integrative Multi-omics and Machine Learning Reveal the Therapeutic Mechanisms of Juanyu-Xiaozhi Formula in Metabolic Dysfunction-associated Steatotic Liver Disease and Hepatic Fibrosis via the AP-1/PPARγ/SCD1 Axis.Journal of clinical and translational hepatology · 2026Article
- Article
- Exercise as a Molecular Therapeutic Tool in MASLD: From Signaling Pathways to Clinical Translation-A Narrative Review.Biomedicines · 2026Review
- Exercise Impacts Liver Disease: Balancing Metabolic and Immune Homeostasis.International journal of biological sciences · 2026Review
- Acetylshikonin mitigates diet-induced MASLD by targeting PPARγ-mediated metabolic dysfunction.Frontiers in pharmacology · 2026Article
- Article
- How Swimming Modulates Inflammatory Pathways in Pain, Neurodegenerative, and Metabolic Disorders.Brain sciences · 2025Review
- Perilipins: key targets for regulating lipid metabolism and alleviating abnormal lipid metabolism through exercise.Diabetology & metabolic syndrome · 2025Review
- Exercise-regulated lipolysis: Its role and mechanism in health and diseases.Journal of advanced research · 2025Review
- Ameliorative Effect of Heat-KilledJournal of microbiology and biotechnology · 2025Article
- N-Lactoyl-Phenylalanine modulates lipid metabolism in microglia/macrophage via the AMPK-PGC1α-PPARγ pathway to promote recovery in mice with spinal cord injury.Journal of neuroinflammation · 2025Article
- Hepatic AKAP1 deficiency exacerbates diet-induced MASLD by enhancing GPAT1-mediated lysophosphatidic acid synthesis.Nature communications · 2025Article
- Effects of moderate intensity exercise on liver metabolism in mice based on multi-omics analysis.Scientific reports · 2024Article
- Chiglitazar ameliorates dehydroepiandrosterone-induced polycystic ovary syndrome in rats.Journal of ovarian research · 2024Article
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundRecent findings elucidated hepatic PPARγ functions as a steatogenic-inducer gene that activates de novo lipogenesis, and is involved in regulation of glucose homeostasis, lipid accumulation, and inflammation response. This study delved into a comprehensive analysis of how PPARγ signaling affects the exercise-induced improvement of insulin resistance (IR) and non-alcoholic fatty liver disease (NAFLD), along with its underlying mechanism.
methodsChronic and acute swimming exercise intervention were conducted in each group mice. IR status was assessed by GTT and ITT assays. Serum inflammatory cytokines were detected by Elisa assays. PPARγ and its target genes expression were detected by qPCR assay. Relative protein levels were quantified via Western blotting. ChIP-qPCR assays were used to detect the enrichment of PPARγ on its target genes promoter.
resultsThrough an exploration of a high-fat diet (HFD)-induced IR and NAFLD model, both chronic and acute swimming exercise training led to significant reductions in body weight and visceral fat mass, as well as hepatic lipid accumulation. The exercise interventions also demonstrated a significant amelioration in IR and the inflammatory response. Meanwhile, swimming exercise significantly inhibited PPARγ and its target genes expression induced by HFD, containing CD36, SCD1 and PLIN2. Furthermore, swimming exercise presented significant modulation on regulatory factors of PPARγ expression and transcriptional activity.
conclusionThe findings suggest that swimming exercise can improve lipid metabolism in IR and NAFLD, possibly through PPARγ signaling in the liver of mice.
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