ArticleNature communications2022
Altered glycolysis triggers impaired mitochondrial metabolism and mTORC1 activation in diabetic β-cells.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.
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Who cites it
74 citing papers in PubMed, 99 citations in OpenAlex.
- Ternary mTOR-targeted conductive nanofibrous scaffolds with bioactive peptides orchestrate immune-metabolic-fibrotic balance for diabetic bone regeneration.Bioactive materials · 2026Article
- Regulation of PDH via cysteine oxidation on DLAT.Nature communications · 2026Article
- Lactobacillus gasseri alleviates type 2 diabetes via modulation of gut microbiota-host metabolic networks.Journal of endocrinological investigation · 2026Article
- Brazilin attenuates methylglyoxal‑induced endothelial injury by enhancing eIF5A hypusination and inhibiting the AMPK/mTOR‑mediated autophagy/apoptosis axisInternational journal of molecular medicine · 2026Article
- Hypoglycemic conditions enhance neonatal β-cell glucose responsiveness via AMPK/mTOR-increased KATP channel density.Endocrinology · 2026Article
- Presenilin-1 controls glycolysis and identity of pancreatic beta cells.Communications biology · 2026Article
- The myokine irisin ameliorates the secretory dysfunction of pancreatic β cells in experimental and human type 2 diabetes.Science advances · 2026Article
- Models of hyperglycaemia in diabetes mellitus and its complications.Nature reviews. Endocrinology · 2026Review
- Timing of Antidiabetic Medication Initiation and Risk of Cardiovascular Events and Mortality.JAMA network open · 2026Article
- Dynamically responsive hydrogel with mechanical stimulation enhances diabetic wound healing via activation of Piezo1-mediated efferocytosis.Bioactive materials · 2026Article
- Glucosamine links hyperglycemia to mTORC1 activation and glucose toxicity in diabetes.JCI insight · 2026Article
- Impaired glucose tolerance and mild diabetes induce β-cell dysfunction in mice.Nature communications · 2026Article
- Contrasting Effects of Chronic Glucokinase Activation and Inhibition on Pancreatic Beta-Cell Function.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Article
- Identification and verification of key genes related to oxidative stress in type 2 diabetes and screening of candidate drugs from Traditional Chinese Medicine.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2026Article
- Everolimus suppresses glucose transporter 3 membrane trafficking to improve therapeutic efficacy of umbilical cord blood-derived mesenchymal stem cell transplantation in diabetic retinopathy.Cell death & disease · 2026Article
- Serum metabolomics of diabetic dogs treated with daily administration of a commercially available lyophilized feces preparation.Veterinary research communications · 2026Article
- Med14 phosphorylation shapes genomic response to GLP-1 agonists.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Suppression of ITPK1 and IPMK activities impairs mTORC1 signaling in pancreatic β-cells and implicates IPbioRxiv : the preprint server for biology · 2026Article
- Human MASLD is a diurnal disease driven by multisystem insulin resistance and reduced insulin availability at night.Cell metabolism · 2026Observational
14 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
Chronic hyperglycaemia causes a dramatic decrease in mitochondrial metabolism and insulin content in pancreatic β-cells. This underlies the progressive decline in β-cell function in diabetes. However, the molecular mechanisms by which hyperglycaemia produces these effects remain unresolved. Using isolated islets and INS-1 cells, we show here that one or more glycolytic metabolites downstream of phosphofructokinase and upstream of GAPDH mediates the effects of chronic hyperglycemia. This metabolite stimulates marked upregulation of mTORC1 and concomitant downregulation of AMPK. Increased mTORC1 activity causes inhibition of pyruvate dehydrogenase which reduces pyruvate entry into the tricarboxylic acid cycle and partially accounts for the hyperglycaemia-induced reduction in oxidative phosphorylation and insulin secretion. In addition, hyperglycaemia (or diabetes) dramatically inhibits GAPDH activity, thereby impairing glucose metabolism. Our data also reveal that restricting glucose metabolism during hyperglycaemia prevents these changes and thus may be of therapeutic benefit. In summary, we have identified a pathway by which chronic hyperglycaemia reduces β-cell function.
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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.