ArticleDiabetologia2015
Disruption of CR6-interacting factor-1 (CRIF1) in mouse islet beta cells leads to mitochondrial diabetes with progressive beta cell failure.
Article in Diabetologia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 24 citations in OpenAlex.
- Role of CR6-Interacting Factor 1 (Crif1) in Cardiac Mitochondrial Structure and Stress-Induced Functional Decline.Korean circulation journal · 2026Article
- Mitochondrial Integrity as the Gatekeeper of Cardiac Stress Adaptation: Insights From CRIF1 Deficiency.Korean circulation journal · 2026Article
- Tanshinone IIA ameliorates pancreatic injury in type 2 diabetic mice by modulating inflammation and endoplasmic reticulum stress via the IL-6/JAK2/STAT3 pathway.Functional & integrative genomics · 2025Article
- Study on the correlation between triglyceride glucose index, triglyceride glucose index to high-density lipoprotein cholesterol ratio, and the risk of diabetes in nonalcoholic fatty liver disease.Frontiers in endocrinology · 2025Article
- Article
- Beneficial Effects of Low-Grade Mitochondrial Stress on Metabolic Diseases and Aging.Yonsei medical journal · 2024Review
- A Defect in Mitochondrial Complex III but Not in Complexes I or IV Causes Early β-Cell Dysfunction and Hyperglycemia in Mice.Diabetes · 2023Article
- Mitoribosome insufficiency in β cells is associated with type 2 diabetes-like islet failure.Experimental & molecular medicine · 2022Article
- Multifunctions of CRIF1 in cancers and mitochondrial dysfunction.Frontiers in oncology · 2022Review
- Hearing Impairment in a Mouse Model of Diabetes Is Associated with Mitochondrial Dysfunction, Synaptopathy, and Activation of the Intrinsic Apoptosis Pathway.International journal of molecular sciences · 2021Article
- Differential roles of GDF15 and FGF21 in systemic metabolic adaptation to the mitochondrial integrated stress response.iScience · 2021Article
- SIRT1 Activation Attenuates the Cardiac Dysfunction Induced by Endothelial Cell-Specific Deletion of CRIF1.Biomedicines · 2021Article
- Review
- The mitochondrial unfolded protein response and mitohormesis: a perspective on metabolic diseasesJournal of molecular endocrinology · 2018Review
- Reduced oxidative capacity in macrophages results in systemic insulin resistance.Nature communications · 2018Article
- Growth differentiation factor 15 is a myomitokine governing systemic energy homeostasis.The Journal of cell biology · 2017Article
- Article
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Authors and funding
18 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aim/hypothesisAlthough mitochondrial oxidative phosphorylation (OxPhos) dysfunction is believed to be responsible for beta cell dysfunction in insulin resistance and mitochondrial diabetes, the mechanisms underlying progressive beta cell failure caused by defective mitochondrial OxPhos are largely unknown.
methodsWe examined the in vivo phenotypes of beta cell dysfunction in beta cell-specific Crif1 (also known as Gadd45gip1)-deficient mice. CR6-interacting factor-1 (CRIF1) is a mitochondrial protein essential for the synthesis and formation of the OxPhos complex in the inner mitochondrial membrane.
resultsCrif1(beta-/-) mice exhibited impaired glucose tolerance with defective insulin secretion as early as 4 weeks of age without defects in islet structure. At 11 weeks of age, Crif1(beta-/-) mice displayed characteristic ultrastructural mitochondrial abnormalities as well as severe glucose intolerance. Furthermore, islet area and insulin content was decreased by approximately 50% compared with wild-type mice. Treatment with the glucoregulatory drug exenatide, a glucagon-like peptide-1 (GLP-1) agonist, was not sufficient to preserve beta cell function in Crif1(beta-/-) mice. CONCLUSIONS/
interpretationOur results indicate that mitochondrial OxPhos dysfunction triggers progressive beta cell failure that is not halted by treatment with a GLP-1 agonist. The Crif1(beta-/-) mouse is a useful model for the study of beta cell failure caused by mitochondrial OxPhos dysfunction.
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