ArticleProceedings of the National Academy of Sciences of the United States of America2023
Hypoxia induces a glycolytic complex in intestinal epithelial cells independent of HIF-1-driven glycolytic gene expression.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2023. 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, 46 citations in OpenAlex.
- Feeding microbes to feed the Gut: inulin reprograms intestinal epithelial metabolism and proliferation through HIF1α.Gut microbes · 2026Review
- Understanding physiological adaptations of pregnancy to the chronic hypoxia of high altitude to inform obstetrical and neonatal care.Physiological reviews · 2026Review
- Colonic metabolomic and transcriptomic alterations in a mouse model of metabolic syndrome.American journal of physiology. Gastrointestinal and liver physiology · 2026Article
- FBP1-Mediated Compartmentalization of Glycolytic Enzyme Complexes Suppresses PKM2 Function to Ameliorate MASLD Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Article
- Glucose Transporter 1 in Health and Disease.MedComm · 2026Review
- HIF-1α drives distinct aspects of hypoxia-induced glucose metabolism in intestinal epithelial cells.The Journal of biological chemistry · 2026Article
- Colonic metabolomic and transcriptomic alterations in a mouse model of metabolic syndrome.bioRxiv : the preprint server for biology · 2026Article
- The return of metabolism: biochemistry and physiology of glycolysis.Biological reviews of the Cambridge Philosophical Society · 2026Review
- Engineering combination nanomedicines to overcome cancer resistance.RSC advances · 2026Review
- Hypoxia-Induced Gut-Brain Axis Remodeling and Insomnia: Mechanisms and Microbiota Adaptive Regulation from a Translational Perspective.Journal of inflammation research · 2026Review
- Hypoxia-inducible factors link inflammation and lipid metabolism in atherosclerotic macrophages.Frontiers in cardiovascular medicine · 2026Review
- Identification of Gestation-Specific Patterns of Physiological, Protein and Cell-Free RNA Injury Markers in a Sheep Model of Regulable Preterm Fetal Hypoxia.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- HIF-1 attenuates high-fiber diet-mediated proliferation and stemness of colonic epithelium.Gut microbes · 2025Article
- Hypoxia increases susceptibility of human intestinal epithelial cells to rotavirus infection through repression of interferon induction.Gut microbes · 2025Article
- Giardia duodenalis stabilizes HIF-1α and induces glycolytic alterations in intestinal epithelial cells.Scientific reports · 2025Article
- Nuclear receptors in health and disease: signaling pathways, biological functions and pharmaceutical interventions.Signal transduction and targeted therapy · 2025Review
- Review
- [Curcumin inhibits lipid metabolism in non-small cell lung cancer by downregulating the HIF-1α pathway].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- Endometrium-derived organoids from cystic fibrosis patients and mice as new models to study disease-associated endometrial pathobiology.Cellular and molecular life sciences : CMLS · 2025Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The metabolic adaptation of eukaryotic cells to hypoxia involves increasing dependence upon glycolytic adenosine triphosphate (ATP) production, an event with consequences for cellular bioenergetics and cell fate. This response is regulated at the transcriptional level by the hypoxia-inducible factor-1(HIF-1)-dependent transcriptional upregulation of glycolytic enzymes (GEs) and glucose transporters. However, this transcriptional upregulation alone is unlikely to account fully for the levels of glycolytic ATP produced during hypoxia. Here, we investigated additional mechanisms regulating glycolysis in hypoxia. We observed that intestinal epithelial cells treated with inhibitors of transcription or translation and human platelets (which lack nuclei and the capacity for canonical transcriptional activity) maintained the capacity for hypoxia-induced glycolysis, a finding which suggests the involvement of a nontranscriptional component to the hypoxia-induced metabolic switch to a highly glycolytic phenotype. In our investigations into potential nontranscriptional mechanisms for glycolytic induction, we identified a hypoxia-sensitive formation of complexes comprising GEs and glucose transporters in intestinal epithelial cells. Surprisingly, the formation of such glycolytic complexes occurs independent of HIF-1-driven transcription. Finally, we provide evidence for the presence of HIF-1α in cytosolic fractions of hypoxic cells which physically interacts with the glucose transporter GLUT1 and the GEs in a hypoxia-sensitive manner. In conclusion, we provide insights into the nontranscriptional regulation of hypoxia-induced glycolysis in intestinal epithelial cells.
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