Evidence map›Paper›PMID 40019670›Full record

ReviewJournal of physiology and biochemistry2025

The impact of high altitude (hypobaric hypoxia) on insulin resistance in humans.

María M Adeva-Andany, Lucia Adeva-Contreras, Natalia Carneiro-Freire, Eva Ameneiros-Rodríguez, Matilde Vila-Altesor, Isabel Calvo-Castro

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of physiology and biochemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed.

  1. Cardiometabolic Risk Factors in Women Exposed to High Altitude.International journal of molecular sciences · 2026
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

María M Adeva-AndanyInternal Medicine Department, Hospital General Juan Cardona, c/ Pardo Bazán s/n, Ferrol, 15406, Spain. magdalena.adeva.andany@sergas.es.
Lucia Adeva-ContrerasSchool of Medicine, Santiago de Compostela University, Santiago de Compostela, Galicia, Spain.
Natalia Carneiro-FreireInternal Medicine Department, Hospital General Juan Cardona, c/ Pardo Bazán s/n, Ferrol, 15406, Spain.
Eva Ameneiros-RodríguezInternal Medicine Department, Hospital General Juan Cardona, c/ Pardo Bazán s/n, Ferrol, 15406, Spain.
Matilde Vila-AltesorInternal Medicine Department, Hospital General Juan Cardona, c/ Pardo Bazán s/n, Ferrol, 15406, Spain.
Isabel Calvo-CastroInternal Medicine Department, Hospital General Juan Cardona, c/ Pardo Bazán s/n, Ferrol, 15406, Spain.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Exposure to hypobaric hypoxia (high altitude) diminishes systemic tissue oxygenation. Tissue hypoxia induces insulin resistance and a metabolic switch that reduces oxidative phosphorylation and glucose storage while enhancing glycolysis. Similarly to hypobaric hypoxia, insulin resistance develops in normal humans undergoing normobaric hypoxia and in patients with obstructive sleep apnea. Following acute exposure to high altitude, insulin resistance returns to baseline values upon returning to sea level or when compensatory mechanisms restore tissue oxygenation. However, insulin resistance persists in subjects unable to achieve sufficient oxygen delivery to tissues. Likewise, long-term residents at high altitude develop persistent insulin resistance when compensatory mechanisms do not attain adequate tissue oxygenation. Among these subjects, insulin resistance may cause clinical complications, such as hypertriglyceridemia, reduced HDL-c, visceral obesity, metabolic dysfunction-associated steatotic liver disease, essential hypertension, type 2 diabetes, subclinical vascular injury, cardiovascular disease, and kidney disease. Impaired tissue oxygenation allows the stabilization of hypoxia-inducible factor-1 (HIF-1), a transcription factor that modulates the transcriptional activity of a number of genes to coordinate the physiological responses to tissue hypoxia. Among them, HIF-1 downregulates PPARG, that codes peroxisome proliferator-activated receptor-gamma (PPAR-γ) and PPARGCA, that codes PPAR-γ coactivator-1α, in order to enable insulin resistance and the metabolic switch from oxidative phosphorylation toward glycolysis.

Indexed as

AltitudeAltitude SicknessHypoxiaInsulin ResistanceHumansHypoxia-Inducible Factor 1, alpha SubunitPPAR gammaHypoxia-Inducible Factor 1, alpha SubunitPPAR gammaCardiovascular diseaseHypoxia-inducible factorsInsulin resistanceKidney diseasePeroxisome proliferator-activated receptor-γPeroxisome proliferator-activated receptor-γ coactivator-1α

Identifiers

What OpenQuestion holds

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Registered trials

None linked

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.