ArticleMolecular metabolism2022
Increased glycolysis affects β-cell function and identity in aging and diabetes.
Article in Molecular metabolism, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 54 citations in OpenAlex.
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- Transcriptional regulation of human NMNAT2: insights from 3D genome sequencing and bioinformatics.The FEBS journal · 2026Article
- Impact of control patterns for the atherogenic index of plasma and its obesity-associated indices on transitions in prediabetes glycemic status: results from the CHARLS national cohort study.Lipids in health and disease · 2026Observational
- SS-31 improves the quality of maternally aged oocytes by ameliorating mitochondrial function and metabolism.Journal of ovarian research · 2026Article
- Cancer progression through the lens of age-induced metabolic reprogramming.Nature reviews. Cancer · 2025Review
- Advanced glycation end products induce inflammaging in periodontal ligament fibroblasts through RAGE/AKT/mTOR/glycolysis pathway.Acta odontologica Scandinavica · 2025Article
- Mitochondrial-encoded peptide MOTS-c prevents pancreatic islet cell senescence to delay diabetes.Experimental & molecular medicine · 2025Article
- Article
- Pyruvate kinase modulates the link between β-cell fructose metabolism and insulin secretion.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- β-Adrenergic Blockers Increase cAMP and Stimulate Insulin Secretion Through a PKA/RYR2/TRPM5 Pathway in Pancreatic β-Cells In Vitro.Pharmacology research & perspectives · 2025Article
- Monocyte CCL2 signaling possibly contributes to increased asthma susceptibility in type 2 diabetes.Scientific reports · 2025Article
- Integrative proteomics and metabolomics analysis of the mechanism of pancreatic β-cell dysfunction in aged mice.Frontiers in endocrinology · 2025Article
- Discovery of Glucose Metabolism-Associated Genes in Neuropathic Pain: Insights from Bioinformatics.International journal of molecular sciences · 2024Article
- Investigation of Metabolic and Inflammatory Disorder in the Aging FGF21 Knockout Mouse.Inflammation · 2024Article
- Targeting β-Cell Plasticity: A Promising Approach for Diabetes Treatment.Current issues in molecular biology · 2024Review
- Effects of kaempherol-3-rhamnoside on metabolic enzymes and AMPK in the liver tissue of STZ-induced diabetes in mice.Scientific reports · 2024Article
- Sildenafil amplifies calcium influx and insulin secretion in pancreatic β cells.Physiological reports · 2024Article
- SIRT1 maintains bone homeostasis by regulating osteoblast glycolysis through GOT1.Cellular and molecular life sciences : CMLS · 2024Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveAge is a risk factor for type 2 diabetes (T2D). We aimed to elucidate whether β-cell glucose metabolism is altered with aging and contributes to T2D.
methodsWe used senescence-accelerated mice (SAM), C57BL/6J (B6) mice, and ob/ob mice as aging models. As a diabetes model, we used db/db mice. The glucose responsiveness of insulin secretion and the [U-
resultsWe identified hyperresponsiveness to glucose and compromised cellular identity as dysfunctional phenotypes shared in common between aged and diabetic mouse β cells. We also observed a metabolic commonality between aged and diabetic β cells: hyperactive glycolysis through the increased expression of nicotinamide mononucleotide adenylyl transferase 2 (Nmnat2), a cytosolic nicotinamide adenine dinucleotide (NAD)-synthesizing enzyme. Got1 KO β cells showed increased glycolysis, β-cell dysfunction, and impaired cellular identity, phenocopying aging and diabetes. Using Got1 KO β cells, we show that attenuation of glycolysis or Nmnat2 activity can restore β-cell function and identity.
conclusionsOur study demonstrates that hyperactive glycolysis is a metabolic signature of aged and diabetic β cells, which may underlie age-related β-cell dysfunction and loss of cellular identity. We suggest Nmnat2 suppression as an approach to counteract age-related T2D.
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