ArticleCell metabolism2019
Preserving Insulin Secretion in Diabetes by Inhibiting VDAC1 Overexpression and Surface Translocation in β Cells.
Article in Cell metabolism, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 papers.
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Who cites it
109 citing papers in PubMed, 161 citations in OpenAlex.
- Association between 1,5-Anhydroglucitol and Acute C Peptide Response to Arginine among Patients with Type 2 Diabetes.Journal of diabetes research · 2020Trial
- A membrane-disruptive action of VBIT-4 challenges its role as a widely used VDAC1 oligomerization inhibitor.eLife · 2026Article
- Revealing the Shared Genetic Architecture of Metabolic Dysfunction-Associated Steatotic Liver Disease-Related Traits Through Genomic Structural Equation Modeling.Genetic epidemiology · 2026Article
- Immune checkpoints and immunoregulation in metabolic diseases and cancers: pathological mechanisms and therapeutic potential.Signal transduction and targeted therapy · 2026Review
- Role of voltage-dependent anion channel 1 in neurodegeneration: Mechanisms, implications, and therapeutic potential.Neural regeneration research · 2026Article
- Increased ADORA1 expression in pancreatic islets coincides with insulin secretory defects in human type 2 diabetes.The Journal of biological chemistry · 2026Article
- Compositional recalibrations of cardiolipin integrate loss of stearoyl-CoA desaturase 1 activity with mitochondrial decay in lipid-laden pancreatic β-cells.Cell communication and signaling : CCS · 2026Article
- Targeting VDAC1 to protect against mitochondria-linked cell death pathways: apoptosis, pyroptosis, ferroptosis, and associated diseases.Apoptosis : an international journal on programmed cell death · 2026Article
- Clotting the Gap Between Mitochondria-Mediated Immunity and Mitochondrial Transfer.Circulation research · 2026Review
- Signaling pathways regulating VDAC1 overexpression associated with apoptosis, pyroptosis, and ferroptosis.Cell communication and signaling : CCS · 2026Article
- A dual-action core-shell microneedle system restores mitochondrial function and accelerates healing in diabetic wounds.Journal of nanobiotechnology · 2026Article
- Signaling architecture of the glucagon-like peptide-1 receptor.The Journal of clinical investigation · 2026Review
- Jiangtang Decoction for Type 2 Diabetes and NAFLD: Integrative AnalysisEndocrine, metabolic & immune disorders drug targets · 2026Article
- Deficiency of SCAMP5 Triggers Pancreatic β-Cell Secretory Dysfunction and Apoptosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Functional recovery of islet β cells in human type 2 diabetes: Transcriptome signatures unveil therapeutic approaches.Science advances · 2025Article
- Single-cell analysis of oxidative phosphorylation protein expression in pancreatic islets in type 2 diabetes.The Journal of endocrinology · 2025Article
- Mitochondrial proteins as biomarkers of cellular senescence and age-associated diseases.Aging · 2025Review
- Dynamic GLUT trafficking at high glucose levels enhances insulin secretion: Dysregulation leads to decreased insulin secretion during type 2 diabetes.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Is the Voltage-Dependent Anion Channel a Major Player in Neurodegenerative Diseases?International journal of molecular sciences · 2025Review
- VDAC1 is a target for pharmacologically induced insulin hypersecretion in β cells.Cell reports · 2025Article
49 more citing papers are in PubMed but not listed here.
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Authors and funding
17 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Type 2 diabetes (T2D) develops after years of prediabetes during which high glucose (glucotoxicity) impairs insulin secretion. We report that the ATP-conducting mitochondrial outer membrane voltage-dependent anion channel-1 (VDAC1) is upregulated in islets from T2D and non-diabetic organ donors under glucotoxic conditions. This is caused by a glucotoxicity-induced transcriptional program, triggered during years of prediabetes with suboptimal blood glucose control. Metformin counteracts VDAC1 induction. VDAC1 overexpression causes its mistargeting to the plasma membrane of the insulin-secreting β cells with loss of the crucial metabolic coupling factor ATP. VDAC1 antibodies and inhibitors prevent ATP loss. Through direct inhibition of VDAC1 conductance, metformin, like specific VDAC1 inhibitors and antibodies, restores the impaired generation of ATP and glucose-stimulated insulin secretion in T2D islets. Treatment of db/db mice with VDAC1 inhibitor prevents hyperglycemia, and maintains normal glucose tolerance and physiological regulation of insulin secretion. Thus, β cell function is preserved by targeting the novel diabetes executer protein VDAC1.
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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.