ArticleMolecular metabolism2020
Klf6 protects β-cells against insulin resistance-induced dedifferentiation.
Article in Molecular metabolism, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 24 citations in OpenAlex.
- Investigational treatments of β-cell failure and replacement.Diabetology international · 2026Review
- Profiling Peripheral Blood with an Optimized, Multiplexed, Single-cell Multiome Approach Supports an Insulin-driven Asthma Subtype.bioRxiv : the preprint server for biology · 2026Article
- The possible renoprotective effect of denatonium benzoate in a rat model of type 2 diabetes: role of Krüppel-like factor 6 (KLF6).Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Pivotal contribution of super-enhancer-driven KLF6 expression to the adipogenesis of human adipose-derived stem cells.Inflammation and regeneration · 2026Article
- Alternative splicing immune signature for detecting HBV-related hepatocellular carcinoma in peripheral blood mononuclear cells.Biochemistry and biophysics reports · 2025Article
- Review
- METRNL represses beta-to-alpha cell trans-differentiation to maintain beta cell function under diabetic metabolic stress in mice.Diabetologia · 2025Article
- Studies on Treatment Within the Scope of Medical Biotechnology for Pancreatic Diseases.Molecular biotechnology · 2025Review
- A mechanism-informed deep neural network enables prioritization of regulators that drive cell state transitions.Nature communications · 2025Article
- A multiorgan map of metabolic, signaling, and inflammatory pathways that coordinately control fasting glycemia in mice.iScience · 2024Article
- The Role of Krüppel-like Factors in Pancreatic Physiology and Pathophysiology.International journal of molecular sciences · 2023Review
- An Overfeeding-Induced Obesity Mouse Model Reveals Necessity for Sin3a in Postnatal Peak β-Cell Mass Acquisition.Diabetes · 2022Article
- Febuxostat Alleviates Allergic Rhinitis by Inhibiting Inflammation and Monocyte Adhesion in Human Nasal Epithelial Cells via Regulating KLF6.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Sitagliptin protects renal glomerular endothelial cells against high glucose-induced dysfunction and injury.Bioengineered · 2022Article
- MiR-200c-3p aggravates gastric cell carcinoma via KLF6.Genes & genomics · 2021Article
- The Anna Karenina Model of β-Cell Maturation in Development and Their Dedifferentiation in Type 1 and Type 2 Diabetes.Diabetes · 2021Article
- 3D quantification of changes in pancreatic islets in mouse models of diabetes type I and II.Disease models & mechanisms · 2020Article
- Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesIn the pathogenesis of type 2 diabetes, development of insulin resistance triggers an increase in pancreatic β-cell insulin secretion capacity and β-cell number. Failure of this compensatory mechanism is caused by a dedifferentiation of β-cells, which leads to insufficient insulin secretion and diabetic hyperglycemia. The β-cell factors that normally protect against dedifferentiation remain poorly defined. Here, through a systems biology approach, we identify the transcription factor Klf6 as a regulator of β-cell adaptation to metabolic stress.
methodsWe used a β-cell specific Klf6 knockout mouse model to investigate whether Klf6 may be a potential regulator of β-cell adaptation to a metabolic stress.
resultsWe show that inactivation of Klf6 in β-cells blunts their proliferation induced by the insulin resistance of pregnancy, high-fat high-sucrose feeding, and insulin receptor antagonism. Transcriptomic analysis showed that Klf6 controls the expression of β-cell proliferation genes and, in the presence of insulin resistance, it prevents the down-expression of genes controlling mature β-cell identity and the induction of disallowed genes that impair insulin secretion. Its expression also limits the transdifferentiation of β-cells into α-cells.
conclusionOur study identifies a new transcription factor that protects β-cells against dedifferentiation, and which may be targeted to prevent diabetes development.
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