ArticleActa diabetologica2024
Downregulation of Sirt3 contributes to β-cell dedifferentiation via FoxO1 in type 2 diabetic mellitus.
Article in Acta diabetologica, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- Sirtuins as Molecular Mediators of Caloric Restriction in the Pancreas: Implications for β-Cell Function, Metabolism, and Longevity.International journal of molecular sciences · 2026Review
- LDHA induces beta cell dedifferentiation in diabetes through metabolic and epigenetic reprogramming.Diabetologia · 2026Article
- Inactivation of the Phosphatase Activity of Soluble Epoxide Hydrolase Modulates SIRT3 and Attenuates Experimental Pulmonary Hypertension.Comprehensive Physiology · 2026Article
- Mechanistic Links Between the Gut Microbiome and Longevity Therapeutics.Biomedicines · 2026Review
- SIRT1 Regulates Iron Metabolism to Attenuate β-Cell Dedifferentiation by Inhibiting FoxO1 Acetylation.Biological trace element research · 2026Article
- Single-Cell RNA Sequencing Shows Exercise ProtectsJournal of diabetes research · 2025Article
- Linking oxidative stress biomarkers to disease progression and antioxidant therapy in hypertension and diabetes mellitus.Frontiers in molecular biosciences · 2025Review
- Targeting β-Cell Plasticity: A Promising Approach for Diabetes Treatment.Current issues in molecular biology · 2024Review
- PAX4 gene delivery improves β-cell function in human islets of Type II diabetes.Regenerative medicine · 2024Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
aimsFoxO1 is an important factor in the β-cell differentiation in type 2 diabetes mellitus (T2DM). Sirt3 is found to be involved in FoxO1 function. This study investigated the role of Sirt3 in the β-cell dedifferentiation and its mechanism.
methodsTwelve-week-old db/db mice and INS1 cells transfected with Sirt3-specific short hairpin RNA (shSirt3) were used to evaluate the dedifferentiation of β-cell. Insulin levels were measured by enzyme linked immunosorbent assay. The proteins of Sirt3, T-FoxO1, Ac-FoxO1 and differentiation indexes such as NGN3, OCT4, MAFA were determined by western blot or immunofluorescence staining. The combination of Sirt3 and FoxO1 was determined by the co-immunoprecipitation assay. The transcriptional activity of FoxO1 was detected by dual luciferase reporter assay.
resultsBoth the in vivo and in vitro results showed that Sirt3 was decreased along with β-cell dedifferentiation and decreased function of insulin secretion under high glucose conditions. When Sirt3 was knocked down in INS1 cells, increased β-cell dedifferentiation and lowered insulin secretion were observed. This effect was closely related to the amount loss and the decreased deacetylation of FoxO1, which resulted in a reduction in transcriptional activity.
conclusionDownregulation of Sirt3 contributes to β-cell dedifferentiation in high glucose via FoxO1. Intervention of Sirt3 may be an effective approach to prevent β-cell failure in T2DM.
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