Evidence map›Paper›PMID 40755371›Full record

ArticleEndocrinology, diabetes & metabolism2025

The Effect of Hyperoxia on Nitric Oxide Metabolism in the Skeletal Muscle of Male Type 2 Diabetic Rats.

Mahdis Mousavi, Sajad Jeddi, Reza Norouzirad, Asghar Ghasemi

Abstract read
In one paragraph

Article in Endocrinology, diabetes & metabolism, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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

4 authors.

Mahdis MousaviEndocrine Physiology Research Center, Research Institute for Endocrine Molecular Biology, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.ORCID https://orcid.org/0009-0007-9099-174X
Sajad JeddiEndocrine Physiology Research Center, Research Institute for Endocrine Molecular Biology, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.ORCID https://orcid.org/0000-0002-3911-6620
Reza NorouziradDepartment of Biochemistry, School of Medicine, Dezful University of Medical Sciences, Dezful, Iran.ORCID https://orcid.org/0000-0002-5046-057X
Asghar GhasemiEndocrine Physiology Research Center, Research Institute for Endocrine Molecular Biology, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.ORCID https://orcid.org/0000-0001-6867-2151

Funding

Shahid Beheshti University of Medical Sciences, Tehran, Iran 43012221-1
6 · The paper itself

Abstract

introductionHypoxia is involved in the pathophysiology of type 2 diabetes (T2D), and oxygen therapy (hyperoxia) has been proposed for managing T2D. As a side effect, hyperoxia increases nitric oxide (NO) metabolism and decreases NO bioavailability. This study aims to investigate the effect of hyperoxia on NO synthases (NOSs), which produce NO from L-arginine and arginase, which degrades L-arginine in the soleus muscle (SM) of rats with T2D.

methodsA combined high-fat diet and a low dose of streptozotocin (30 mg/kg) were used to induce T2D in rats. Rats with T2D were divided into four groups (n = 6/group): Control rats exposed to normoxia (Control), control rats exposed to hyperoxia (C + HOX), diabetic rats exposed to normoxia (T2D) and diabetic rats exposed to hyperoxia (T2D + HOX). The hyperoxia and the control groups received 95% and 21% oxygen for 35 days, respectively. SM was isolated at day 35, and the protein levels of endothelial NOS (eNOS), inducible NOS (iNOS), arginase, as well as tissue concentrations of lactate and NO metabolites (nitrate+nitrite = NOx) were measured.

resultsCompared to T2D, T2D + HOX rats had lower lactate concentration by 38% (p = 0.009) and NOx concentration by 23% (p = 0.011) in SM. In SM of rats with T2D, hyperoxia decreased eNOS protein by 46.2% (1.4 ± 0.13 vs. 2.6 ± 0.2 ng/mg protein, p = 0.002) and increased arginase protein by 2.3-fold (1.04 ± 0.05 vs. 0.31 ± 0.07 ng/mg protein, p < 0.001) but did not affect iNOS protein. Hyperoxia did not affect lactate concentration, eNOS and iNOS in SM of control rats but decreased NOx concentration by 25% (p = 0.003).

conclusionHyperoxia decreased NO bioavailability in SM of rats with T2D; this effect was associated with decreased eNOS and increased arginase protein levels. These findings suggest that oxygen therapy in diabetic rats may decrease NO bioavailability as a potential side effect.

Indexed as

Diabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2HyperoxiaMuscle, SkeletalNitric OxideAnimalsArginaseMaleNitric Oxide Synthase Type IINitric Oxide Synthase Type IIIRatsRats, WistarArginaseNitric OxideNitric Oxide Synthase Type IINitric Oxide Synthase Type IIIarginasehyperoxianitric oxidetype 2 diabetes

Identifiers

PMID40755371
PMCPMC12319423

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

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 Socratic graph.