ArticleWorld journal of gastroenterology2022
Peroxisome proliferator-activated receptor-alpha activation and dipeptidyl peptidase-4 inhibition target dysbiosis to treat fatty liver in obese mice.
Article in World journal of gastroenterology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 22 citations in OpenAlex.
- DPP-4 inhibitors in drug-resistant epilepsy: a hypothesized mechanism via the gut microbiota-short-chain fatty acids-glucagon-like peptide-1 axis.Frontiers in immunology · 2026Review
- Sinensetin ameliorates established high-fat diet-induced liver injury and intestinal barrier dysfunction through the mitophagy/TLR4/MAPK signaling pathway.Frontiers in nutrition · 2026Article
- Vildagliptin modulates the microbiota and induces an immunometabolic profile compatible with neuroprotection in type 2 diabetes.Scientific reports · 2025Article
- Gut-Liver Axis: The Role of Intestinal Microbiota and Their Metabolites in the Progression of Metabolic Dysfunction-Associated Steatotic Liver Disease.Gut and liver · 2025Review
- Bidirectional Interactions Between the Gut Microbiota and Incretin-Based Therapies.Life (Basel, Switzerland) · 2025Review
- Probing and manipulating the gut microbiome with chemistry and chemical tools.Gut microbiome (Cambridge, England) · 2025Review
- Dietary Influences on Gut Microbiota and Their Role in Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD).Nutrients · 2024Review
- Article
- Review on the role of nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome pathway in diabetes: mechanistic insights and therapeutic implications.Inflammopharmacology · 2024Review
- Mechanism of Metabolic Dysfunction-associated Steatotic Liver Disease: Important role of lipid metabolism.Journal of clinical and translational hepatology · 2024Review
- Time-dependent impact of a high-fat diet on the intestinal barrier of male mice.World journal of methodology · 2024Article
- Association of metabolic-dysfunction associated steatotic liver disease with polycystic ovary syndrome.iScience · 2024Review
- Review
- Peroxisome proliferator-activated receptors as targets to treat metabolic diseases: Focus on the adipose tissue, liver, and pancreas.World journal of gastroenterology · 2023Review
- The PPARα Regulation of the Gut Physiology in Regard to Interaction with Microbiota, Intestinal Immunity, Metabolism, and Permeability.International journal of molecular sciences · 2022Review
- The Related Metabolic Diseases and Treatments of Obesity.Healthcare (Basel, Switzerland) · 2022Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundObesity and comorbidities onset encompass gut dysbiosis, altered intestinal permeability, and endotoxemia. Treatments that target gut dysbiosis can cope with obesity and nonalcoholic fatty liver disease (NAFLD) management. Peroxisome proliferator-activated receptor (PPAR)-alpha activation and dipeptidyl-peptidase-4 (DPP-4) inhibition alleviate NAFLD, but the mechanism may involve gut microbiota modulation and merits further investigation.
aimTo address the effects of PPAR-alpha activation and DPP-4 inhibition (isolated or combined) upon the gut-liver axis, emphasizing inflammatory pathways in NAFLD management in high-fat-fed C57BL/6J mice.
methodsMale C57BL/6J mice were fed a control diet (C, 10% of energy as lipids) or a high-fat diet (HFD, 50% of energy as lipids) for 12 wk, when treatments started, forming the groups: C, HF, HFA (HFD + PPAR-alpha agonist WY14643, 2.5 mg/kg body mass), HFL (HFD + DPP-4 inhibitor linagliptin, 15 mg/kg body mass), and HFC (HFD + the combination of WY14643 and linagliptin).
resultsThe HFD was obesogenic compared to the C diet. All treatments elicited significant body mass loss, and the HFC group showed similar body mass to the C group. All treatments tackled oral glucose intolerance and raised plasma glucagon-like peptide-1 concentrations. These metabolic benefits restored
conclusionPPAR alpha activation and DPP-4 inhibition (isolated or combined) tackled NAFLD in diet-induced obese mice by restoration of gut-liver axis. The reestablishment of the intestinal barrier and the rescued phylogenetic gut bacteria distribution mitigated liver steatosis through anti-inflammatory signals. These results can cope with NAFLD management by providing pre-clinical evidence that drugs used to treat obesity comorbidities can help to alleviate this silent and harmful liver disease.
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