NMN plus glucose in mice under hypobaric hypoxia: tissue injury and iron overload
In mice under hypobaric hypoxia, a combined regimen of nicotinamide mononucleotide (NMN) and glucose reduced tissue injury and body weight loss and counteracted metabolic disruptions; the abstract links these effects to iron overload, oxidative stress and ferroptosis-related metabolic changes. [1]
Automatic summary · not editorially reviewed
The key findings
In mice under hypobaric hypoxia, a combined regimen of NMN and glucose attenuated tissue injury and prevented body weight loss, according to the abstract. [1]
The authors identified hypobaric-hypoxia-induced iron overload and oxidative stress as key pathological drivers, with glutathione depletion and lipid peroxidation across multiple tissues. [1]
NMN plus glucose reversed ferroptosis-associated metabolic alterations and alleviated mitochondrial dysfunction, the abstract reports. [1]
The source at a glance
- Study type / format
- Preclinical mouse study (abstract).
- Population / context
- Mice under hypobaric hypoxia.
- Summary based on
- Study abstract
- Original publication
- August 21, 2026
Hypobaric hypoxia in mice and the NMN-glucose regimen
The abstract describes mice kept under hypobaric hypoxia (HH), a simulated high-altitude condition. The tested intervention was a combined regimen of nicotinamide mononucleotide (NMN) and glucose. According to the abstract, this combination attenuated tissue injury and prevented body weight loss in these mice. The authors frame the work as a search for metabolic interventions for extreme high-altitude environments.
Supporting source [1]
Iron overload and oxidative stress as described drivers
Using a multi-tissue atlas covering metabolome, lipidome, proteome and phenotypic profiles, the authors identified HH-induced iron overload and oxidative stress as key pathological drivers. They describe an HH-induced, transferrin-inspired iron delivery that caused iron overload and oxidative stress, together with glutathione depletion and lipid peroxidation across multiple tissues. Protein levels of the ferroptosis markers ACSL4, GPX4 and FSP1 showed no significant changes, though the authors state they cannot rule out altered activity of these proteins.
Supporting source [1]
Metabolic reversal and mitochondrial findings in the abstract
The abstract reports that NMN plus glucose significantly counteracted metabolic disruptions across multiple tissues. It further states that the combination reversed ferroptosis-associated metabolic alterations and alleviated mitochondrial dysfunction. The authors conclude that NMN combined with glucose mitigates HH-induced multi-organ injury by suppressing ferroptosis through metabolic reprogramming, and they suggest therapeutic potential for high-altitude hypoxia. These are findings in mice; the abstract does not report human outcomes.
Supporting source [1]
How to interpret this
This is an abstract; the full text was not reviewed. The work is a mouse study under hypobaric hypoxia, and the abstract reports no human data. Protein levels of ferroptosis markers were unchanged, and the authors note they cannot rule out activity changes. The abstract does not report sample sizes, follow-up duration or effect sizes.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Tan F, Huang X, Mao X, Wang Y, Wang X, Tang F, Chen X, Mao R, Gong X, Chen L, Di LJ, Zhang S, Zeng J, Lin SH. · europepmc.org · August 21, 2026