ArticleBiomolecules2021
Gut Metabolite Trimethylamine N-Oxide Protects INS-1 β-Cell and Rat Islet Function under Diabetic Glucolipotoxic Conditions.
Article in Biomolecules, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.
- Effects of different hypoglycaemic drugs on beta-cell function in type 2 diabetes mellitus: a systematic review and network meta-analysis.European journal of medical research · 2025Pooled it
- Gut microbiota-generated trimethylamineAmerican journal of physiology. Endocrinology and metabolism · 2026Trial
- Article
- β-cell FMO3-produced TMAO prevents NF-κB-mediated senescence and inflammation in ageing and diabetic conditions.Nature communications · 2026Article
- MEF2D impairs mitochondrial respiration, glucose-stimulated insulin secretion, and survival in INS-1 β-cells.bioRxiv : the preprint server for biology · 2026Article
- Nr4a1 β-cell specific deletion impairs glucose tolerance in female mice.American journal of physiology. Endocrinology and metabolism · 2026Article
- Establishment of a mouse model of TMAO-induced cardiac injury and application of MICT intervention.Animal models and experimental medicine · 2026Article
- Role of Gut Microbiota in Diabetic HFpEF: Mechanisms and Therapeutic Implications.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Review
- TMAO and diabetes: from the gut feeling to the heart of the problem.Nutrition & diabetes · 2025Review
- Gut Microbiota Metabolite TMAO and Adolescent Cardiometabolic Health: A Cross-sectional Analysis.Journal of the Endocrine Society · 2025Article
- Unraveling the role of the gut microbiome in pregnancy disorders: insights and implications.Frontiers in cellular and infection microbiology · 2025Review
- Gut Microbe-Generated Metabolite Trimethylamine-N-Oxide and Ischemic Stroke.Biomolecules · 2024Review
- Trimethylamine N-oxide impairs β-cell function and glucose tolerance.Nature communications · 2024Article
- Article
- Trimethylamine N-Oxide Improves Exercise Performance by Reducing Oxidative Stress through Activation of the Nrf2 Signaling Pathway.Molecules (Basel, Switzerland) · 2024Article
- Probiotic for Pancreatic β-Cell Function in Type 2 Diabetes: A Randomized, Double-Blinded, Placebo-Controlled Clinical Trial.Diabetes therapy : research, treatment and education of diabetes and related disorders · 2023Article
- Bioavailable Microbial Metabolites of Flavanols Demonstrate Highly Individualized Bioactivity on In Vitro β-Cell Functions Critical for Metabolic Health.Metabolites · 2023Article
- The Pancreatic Beta Cell: Editorial.Biomolecules · 2023Article
- Recent insights of obesity-induced gut and adipose tissue dysbiosis in type 2 diabetes.Frontiers in molecular biosciences · 2023Review
- NMR-Based Metabolomic Analysis for the Effects of Trimethylamine N-Oxide Treatment on C2C12 Myoblasts under Oxidative Stress.Biomolecules · 2022Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Serum accumulation of the gut microbial metabolite trimethylamine N-oxide (TMAO) is associated with high caloric intake and type 2 diabetes (T2D). Impaired pancreatic β-cell function is a hallmark of diet-induced T2D, which is linked to hyperglycemia and hyperlipidemia. While TMAO production via the gut microbiome-liver axis is well defined, its molecular effects on metabolic tissues are unclear, since studies in various tissues show deleterious and beneficial TMAO effects. We investigated the molecular effects of TMAO on functional β-cell mass. We hypothesized that TMAO may damage functional β-cell mass by inhibiting β-cell viability, survival, proliferation, or function to promote T2D pathogenesis. We treated INS-1 832/13 β-cells and primary rat islets with physiological TMAO concentrations and compared functional β-cell mass under healthy standard cell culture (SCC) and T2D-like glucolipotoxic (GLT) conditions. GLT significantly impeded β-cell mass and function by inducing oxidative and endoplasmic reticulum (ER) stress. TMAO normalized GLT-mediated damage in β-cells and primary islet function. Acute 40µM TMAO recovered insulin production, insulin granule formation, and insulin secretion by upregulating the IRE1α unfolded protein response to GLT-induced ER and oxidative stress. These novel results demonstrate that TMAO protects β-cell function and suggest that TMAO may play a beneficial molecular role in diet-induced T2D conditions.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.