Evidence map›Paper›PMID 18437348›Full record

ArticleDiabetologia2008

Exercise restores endothelial function independently of weight loss or hyperglycaemic status in db/db mice.

F Moien-Afshari, S Ghosh, S Elmi, M M Rahman, N Sallam, M Khazaei, T J Kieffer, R W Brownsey, I Laher

Erratum issuedOpen access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Diabetologia, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
6.6field-weighted citation impact, top 3% of its field
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

63 citing papers in PubMed, 106 citations in OpenAlex.

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  15. Impairment of Flow-Sensitive Inwardly Rectifying KArteriosclerosis, thrombosis, and vascular biology · 2020
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3 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

  • Erratum issued
    Elmi, S [added]; Rahman, M M [added]; Sallam, N [added]
5 · Who and what money

Authors and funding

9 authors at 3 institutions in 2 countries.

F Moien-AfshariDepartment of Pharmacology and Therapeutics, University of British Columbia, Vancouver, BC, V6T 1Z3, Canada.
S Ghosh
S Elmi
M M Rahman
N Sallam
M Khazaei
T J Kieffer
R W Brownsey
I Laher
University of British Columbia · CAChild and Family Research Institute · CAIsfahan University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aims/hypothesisExercise ameliorates oxidative stress-mediated diabetic vascular endothelial dysfunction through poorly defined mechanisms. We hypothesised that, in addition to improving metabolic parameters, upregulation of antioxidants such as superoxide dismutase (SOD) mediates exercise-induced reductions of oxidative stress and increased nitric oxide (NO) bioavailability, and also restores vasodilatation.

methodsType 2 diabetic db/db and normoglycaemic wild-type mice were exercised at moderate intensity for 1 h a day for 7 weeks, leading to a 10% body weight loss. Sedentary animals or those undergoing a low-intensity exercise regimen causing non-significant weight loss were also used. We examined aortic endothelial cell function, NO bioavailability and various biomarkers of oxidative stress.

resultsModerate-intensity exercise lowered body weight, increased mitochondrial manganese SOD (MnSOD) and both total and phosphorylated (Ser1177) endothelial nitric oxide synthase (eNOS) protein production; it also reduced whole-body (plasma 8-isoprostane) and tissue oxidative stress (nitrotyrosine immunostaining or protein carbonyl levels in the aorta). Low-intensity exercise did not alter body weight; however, it upregulated cytosolic Cu/Zn-SOD instead of MnSOD, and still demonstrated all the above benefits in the db/db aorta. Importantly, both exercise protocols improved endothelial-dependent vasodilatation and NO bioavailability without altering hyperglycaemic status in db/db mice. CONCLUSIONS/

interpretationExercise reverses diabetic vascular endothelial dysfunction independently of improvements in body weight or hyperglycaemia. Our data suggest that upregulation of eNOS and specific SOD isoforms could play important roles in improving NO bioavailability, as well as in reversing endothelial dysfunction in type 2 diabetes patients through lifestyle modifications in the management of diabetes.

Indexed as

Adipose TissueAnimalsAntioxidantsAortaBody WeightDiabetes Mellitus, Type 2Diabetic AngiopathiesEndothelial CellsHyperglycemiaIsometric ContractionLipidsMaleMiceMice, Mutant StrainsNitric OxideNitric Oxide Synthase Type IIAntioxidantsLipidsNitric OxideNitric Oxide Synthase Type IINitric Oxide Synthase Type IIINitritesNos3 protein, mouseSuperoxide Dismutase

Identifiers

PMID18437348
OpenAlexW1968849802

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.