ArticleFrontiers in physiology2019
The Bile Acid TUDCA Improves Beta-Cell Mass and Reduces Insulin Degradation in Mice With Early-Stage of Type-1 Diabetes.
Article in Frontiers in physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
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Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.
- TUDCA and 4-PBA in Preclinical Models of Beta-Cell Secretory Failure: A Systematic Review and Bayesian Meta-Analysis.International journal of molecular sciences · 2026Pooled it
- Translating gut microbiome research into therapies for type 1 diabetes.Experimental physiology · 2026Review
- Regulation of Endoplasmic Reticulum Stress Suppresses Early Pro-Tumorigenic Events During N-Nitrosodiethylamine-Induced Hepatocarcinogenesis.Journal of biochemical and molecular toxicology · 2026Article
- FXR and BET signaling orchestrate to protect β cells.bioRxiv : the preprint server for biology · 2026Article
- Use of Small Organic Molecules to Improve Pancreatic Beta Cell Resilience to IAPP-Induced Proteotoxic Stress.International journal of molecular sciences · 2026Review
- Article
- Pharmacological activation of SERCA2 reverses ER calcium dysregulation and depression-like behaviors in hyperglycemic mice.Scientific reports · 2025Article
- Lactococcus lactis-HSP65 requires TLR2 to induce tolerogenic dendritic cells and confer protection against type 1 diabetes in a murine model.Cellular and molecular life sciences : CMLS · 2025Article
- Hepatocyte-Specific ApoJ Knockout Improves Metabolic Profiles in the Liver of Diabetic Mice.Metabolites · 2025Article
- Renoprotective Effects of Phloretin and TUDCA via Simultaneous Inhibition of TLR4/MyD88/NF-κB and BiP/PERK/CHOP Pathways in AKI Under Diabetic Condition.Applied biochemistry and biotechnology · 2025Article
- Restoration of intestinal secondary bile acid synthesis: A potential approach to improve pancreatic β cell function in type 1 diabetes.Cell reports. Medicine · 2025Article
- From Microbes to Metabolites: Advances in Gut Microbiome Research in Type 1 Diabetes.Metabolites · 2025Review
- Regulatory T cell dysfunction and immunotherapeutic breakthroughs in type 1 diabetes.Frontiers in endocrinology · 2025Review
- Review
- Nrf2 Signaling Pathway as a Key to Treatment for Diabetic Dyslipidemia and Atherosclerosis.International journal of molecular sciences · 2024Review
- The gut microbiota intervenes in glucose tolerance and inflammation by regulating the biosynthesis of taurodeoxycholic acid and carnosine.Frontiers in cellular and infection microbiology · 2024Article
- Endothelial Dysfunction in Diabetes Mellitus: New Insights.International journal of molecular sciences · 2023Review
- Review
- Elevated Bile Acid Is Associated with Worsened Impaired Glucose Homeostasis in Pancreatic Ductal Adenocarcinoma Patients with Extrahepatic Cholestasis through Increased Hepatic Insulin Clearance.Journal of clinical medicine · 2023Article
- Effects of Tauroursodeoxycholic Acid and 4-Phenylbutyric Acid on Selenium Distribution in Mice Model with Type 1 Diabetes.Biological trace element research · 2023Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Type 1 diabetes (T1D) is characterized by impairment in beta-cell mass and insulin levels, resulting in hyperglycemia and diabetic complications. Since diagnosis, appropriate control of glycaemia in T1D requires insulin administration, which can result in side effects, such as hypoglycemia. In this sense, some bile acids have emerged as new therapeutic targets to treat T1D and T2D, as well as metabolic diseases. The taurine conjugated bile acid, tauroursodeoxycholic (TUDCA) reduces the incidence of T1D development and improves glucose homeostasis in obese and T2D mice. However, its effects in early-stage of T1D have not been well explored. Therefore, we have assessed the effects of TUDCA on the glycemic control of mice with early-stage T1D. To achieve this, C57BL/6 mice received intraperitoneal administration of streptozotocin (STZ, 40 mg/kg) for 5 days. Once diabetes was confirmed in the STZ mice, they received TUDCA treatment (300 mg/kg) or phosphate buffered saline (PBS) for 24 days. After 15 days of treatment, the STZ+TUDCA mice showed a 43% reduction in blood glucose, compared with the STZ group. This reduction was likely due to an increase in insulinemia. This increase in insulinemia may be explained, at least in part, by a reduction in hepatic IDE activity and, consequently, reduction on insulin clearance, as well as an increase in beta-cell mass and a higher beta-cell number per islet. Also, the groups did not present any alterations in insulin sensitivity. All together, these effects contributed to the improvement of glucose metabolism in T1D mice, pointing TUDCA as a potential therapeutic agent for the glycemic control in early-stage of T1D.
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