ArticleDiabetes2012
Bile acids acutely stimulate insulin secretion of mouse β-cells via farnesoid X receptor activation and K(ATP) channel inhibition.
Article in Diabetes, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
80 citing papers in PubMed, 157 citations in OpenAlex.
- Serum Fibroblast Growth Factor 19 and Total Bile Acid Concentrations Are Potential Biomarkers of Hepatocellular Carcinoma in Patients with Type 2 Diabetes Mellitus.BioMed research international · 2020Trial
- Weight loss induced by Roux-en-Y gastric bypass but not laparoscopic adjustable gastric banding increases circulating bile acids.The Journal of clinical endocrinology and metabolism · 2013Trial
- FXR and BET signaling orchestrate to protect β cells.bioRxiv : the preprint server for biology · 2026Article
- Declining FXR expression coordinates neonatal beta cell mass development with microbial bile acid metabolism maturation in mice.Diabetologia · 2026Article
- Genetic variance in the murine defensin locus modulates glucose homeostasis.The EMBO journal · 2025Article
- From cholesterol to glucose: uncovering how statins induce β-cell dysfunction to promote type 2 diabetes.The Journal of endocrinology · 2025Review
- The role of the farnesoid X receptor in diabetes and its complications.Molecular and cellular biochemistry · 2025Review
- Review
- Bile acid metabolism in type 2 diabetes mellitus.Nature reviews. Endocrinology · 2025Review
- Bile acids as therapeutic agents.Frontiers in pharmacology · 2025Review
- Bile acid signaling in the regulation of whole body metabolic and immunological homeostasis.Science China. Life sciences · 2024Review
- FXR-mediated epigenetic regulation of GLP-1R expression contributes to enhanced incretin effect in diabetes after RYGB.Journal of cellular and molecular medicine · 2024Article
- Bile salt signaling and bile salt-based therapies in cardiometabolic disease.Clinical science (London, England : 1979) · 2024Article
- Research progress on the relationship between bile acid metabolism and type 2 diabetes mellitus.Diabetology & metabolic syndrome · 2023Review
- The role of GLUT2 in glucose metabolism in multiple organs and tissues.Molecular biology reports · 2023Review
- Physical properties of food or bile redirection do not contribute to the intestinal adaptations after Roux-en-Y Gastric Bypass in rats.Obesity science & practice · 2023Article
- Hepatokines, bile acids and ketone bodies are novel Hormones regulating energy homeostasis.Frontiers in endocrinology · 2023Review
- Review
- Chlorothalonil exposure induces "liver-gut axis" disorder in mice.Acta biochimica et biophysica Sinica · 2022Article
- Article
20 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Type 2 diabetes mellitus is associated with alterations in bile acid (BA) signaling. The aim of our study was to test whether pancreatic β-cells contribute to BA-dependent regulation of glucose homeostasis. Experiments were performed with islets from wild-type, farnesoid X receptor (FXR) knockout (KO), and β-cell ATP-dependent K(+) (K(ATP)) channel gene SUR1 (ABCC8) KO mice, respectively. Sodium taurochenodeoxycholate (TCDC) increased glucose-induced insulin secretion. This effect was mimicked by the FXR agonist GW4064 and suppressed by the FXR antagonist guggulsterone. TCDC and GW4064 stimulated the electrical activity of β-cells and enhanced cytosolic Ca(2+) concentration ([Ca(2+)](c)). These effects were blunted by guggulsterone. Sodium ursodeoxycholate, which has a much lower affinity to FXR than TCDC, had no effect on [Ca(2+)](c) and insulin secretion. FXR activation by TCDC is suggested to inhibit K(ATP) current. The decline in K(ATP) channel activity by TCDC was only observed in β-cells with intact metabolism and was reversed by guggulsterone. TCDC did not alter insulin secretion in islets of SUR1-KO or FXR-KO mice. TCDC did not change islet cell apoptosis. This is the first study showing an acute action of BA on β-cell function. The effect is mediated by FXR by nongenomic elements, suggesting a novel link between FXR activation and K(ATP) channel inhibition.
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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.