ArticlePloS one2018
Lactobacillus plantarum reverse diabetes-induced Fmo3 and ICAM expression in mice through enteric dysbiosis-related c-Jun NH2-terminal kinase pathways.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.
- Role of gut microbiota in type 2 diabetes pathophysiology.EBioMedicine · 2020Pooled it
- Trial
- β-cell FMO3-produced TMAO prevents NF-κB-mediated senescence and inflammation in ageing and diabetic conditions.Nature communications · 2026Article
- Review
- Trimethylamine N-Oxide (TMAO) Acts as Inhibitor of Endothelial Nitric Oxide Synthase (eNOS) and Hampers NO Production and Acetylcholine-Mediated Vasorelaxation in Rat Aortas.Antioxidants (Basel, Switzerland) · 2025Article
- Managing Type 2 Diabetes Mellitus via the Regulation of Gut Microbiota: A Chinese Medicine Perspective.Nutrients · 2024Review
- Curcumin and Gut Microbiota: A Narrative Overview with Focus on Glycemic Control.International journal of molecular sciences · 2024Review
- Diabetes Mellitus and Gastric Cancer: Correlation and Potential Mechanisms.Journal of diabetes research · 2023Review
- Mechanism and application ofFrontiers in public health · 2023Review
- The Anti-Inflammatory Effect of Novel Antidiabetic Agents.Life (Basel, Switzerland) · 2022Review
- Characteristics of Gut Microbiota in Female Patients with Diabetic Microvascular Complications.Journal of diabetes research · 2022Article
- Can diet modulate trimethylamine N-oxide (TMAO) production? What do we know so far?European journal of nutrition · 2021Review
- Modulating the Microbiota as a Therapeutic Intervention for Type 2 Diabetes.Frontiers in endocrinology · 2021Review
- Probiotics, Prebiotics and Synbiotics-A Promising Strategy in Prevention and Treatment of Cardiovascular Diseases?International journal of molecular sciences · 2020Review
- Probiotics supplementation and insulin resistance: a systematic review.Diabetology & metabolic syndrome · 2020Review
- Considerations for Gut Microbiota and Probiotics in Patients with Diabetes Amidst the Covid-19 Pandemic: A Narrative Review.Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists · 2020Review
- Anti-Diabetic Effects of Allulose in Diet-Induced Obese Mice via Regulation of mRNA Expression and Alteration of the Microbiome Composition.Nutrients · 2020Article
- Effects ofMedicina (Kaunas, Lithuania) · 2019Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetes mellitus (DM) is characterized by increased fatality associated with the atherogenetic process. Circulating trimethylamine-N-oxide (TMAO) levels are closely associated with atherosclerosis. The flavin mono-oxygenase family (Fmo) members oxidize trimethylamine (TMA) to TMAO. The effect and the regulatory mechanism of intestinal microflora on diabetes-induced Fmo3 and intercellular adhesion molecule (ICAM) expression were examined in streptozotocin-induced diabetic mice (STZDM) and Akita mice (C57BL/6J-Ins2Akita). STZDM-JNK1-/- and Ins2Akita-JNK1-/- mice were produced and used to study the role of pJNK in the regulatory mechanisms. Diabetic mice exhibited decreased Lactobacilli growth and reactive oxygen species (ROS) production in the intestinal mucosa; increased levels of pJNK and iNOS proteins in the intestinal mucosa; increased levels of serum nitrate, IL-1β, and TNF-α expression in Kupffer cells; increased Fmo3 expression in the liver; and increased ICAM expression in the aorta. Reversal of diabetes-induced enteric dysbiosis by prebiotic (FOS) or probiotic (dead L. plantarum) treatment decreased diabetes-induced pJNK and iNOS expression in the intestine, Fmo3 expression in the liver, IL-1β expression in Kupffer cells, and ICAM expression in the aorta and liver. Ins2Akita-JNK1-/- and STZDM-JNK1-/- mice demonstrated decreased levels of serum NO, IL-1β expression in Kupffer cells, Fmo3 expression in the liver, and ICAM expression in the aorta. GF mice cohoused with DM mice demonstrated an increase in ICAM expression in the liver. In conclusion, diabetes induced the expression of both Fmo3 and ICAM expression and possible vascular impairment through enteric dysbiosis. Diabetes-induced Fmo3 and ICAM expression could be reversed by pJNK inhibition or by correcting enteric dysbiosis.
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