ArticleCell metabolism2026
Red blood cells serve as a primary glucose sink to improve glucose tolerance at altitude.
Article in Cell metabolism, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
7 citing papers in PubMed.
- HbA1c reconsidered: glycated haemoglobin in the era of dynamic erythrocyte glucose metabolism.Acta diabetologica · 2026Article
- Article
- Advancing high-altitude medicine: a model for the future.Signal transduction and targeted therapy · 2026Review
- When Red Blood Cells Meet Carbon Monoxide: Yin and Yang in Medicines and Pharmaceuticals.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Article
- Association between glycated hemoglobin A1c and diabetic retinopathy in adults with type 2 diabetes mellitus residing at high altitudes.Frontiers in endocrinology · 2026Article
- Combining exercise and hypoxia for brain health: from elite athlete altitude training camps to clinical applications.AIMS neuroscience · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors.
Funding
Abstract
High-altitude conditions improve glucose tolerance and reduce diabetes risk, but the physiological mechanism is not well understood. Using mouse models, we found that hypoxia alone robustly improved glucose tolerance and that the effect persisted for weeks after returning to normal oxygen levels. PET/CT imaging suggested a significant, unknown glucose sink beyond major internal organs. We hypothesized that hypoxia-induced red blood cells (RBCs) serve as this sink. Manipulating RBC numbers through phlebotomy or transfusion directly altered blood glucose, establishing RBCs as necessary and sufficient for this effect. In chronic hypoxia, RBCs showed a sustained ∼3-fold increase in glucose uptake and ∼2-fold increase in GLUT1 protein abundance, specifically in newly synthesized RBCs, which ultimately contributes to increased glycolytic flux toward 2,3-diphosphoglycerate (2,3-DPG). Mechanistically, acute hypoxia displaces GAPDH from inhibitory band 3 binding through competitive interactions with deoxyhemoglobin, thereby boosting glycolytic flux and driving 2,3-DPG production. We also found that hypoxia or our small-molecule hypoxia mimetic, HypoxyStat, rescued hyperglycemia in mouse models of type 1 and type 2 diabetes. Our findings identify RBCs as key regulators of systemic glucose metabolism, highlighting a novel therapeutic approach for hyperglycemic disorders.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.