Evidence map›Paper›PMID 27585884›Full record

ArticleDisease models & mechanisms2016

Poor maternal nutrition and accelerated postnatal growth induces an accelerated aging phenotype and oxidative stress in skeletal muscle of male rats.

Jane L Tarry-Adkins, Denise S Fernandez-Twinn, Jian Hua Chen, Iain P Hargreaves, Viruna Neergheen, Catherine E Aiken, Susan E Ozanne

Open access · goldAbstract read
In one paragraph

Article in Disease models & mechanisms, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
15.0field-weighted citation impact, top 1% 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

36 citing papers in PubMed, 62 citations in OpenAlex.

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  6. Research progress on the effects of adverse exposure during pregnancy on skeletal muscle function in the offspring.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2023
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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

7 authors at 2 institutions in 1 country.

Jane L Tarry-AdkinsUniversity of Cambridge Metabolic Research Laboratories and MRC Metabolic Diseases Unit, Wellcome Trust-MRC Institute of Metabolic Science, Addenbrooke's Treatment Centre, Addenbrooke's Hospital, Hills Road, Cambridge CB2 OQQ, UK janeadkins@googlemail.com.ORCID 0000-0001-9569-6132
Denise S Fernandez-TwinnUniversity of Cambridge Metabolic Research Laboratories and MRC Metabolic Diseases Unit, Wellcome Trust-MRC Institute of Metabolic Science, Addenbrooke's Treatment Centre, Addenbrooke's Hospital, Hills Road, Cambridge CB2 OQQ, UK.
Jian Hua ChenUniversity of Cambridge Metabolic Research Laboratories and MRC Metabolic Diseases Unit, Wellcome Trust-MRC Institute of Metabolic Science, Addenbrooke's Treatment Centre, Addenbrooke's Hospital, Hills Road, Cambridge CB2 OQQ, UK.
Iain P HargreavesNeurometabolic Unit, National Hospital, University College London, London WC1N 3BG, UK.
Viruna NeergheenNeurometabolic Unit, National Hospital, University College London, London WC1N 3BG, UK.
Catherine E AikenUniversity of Cambridge Metabolic Research Laboratories and MRC Metabolic Diseases Unit, Wellcome Trust-MRC Institute of Metabolic Science, Addenbrooke's Treatment Centre, Addenbrooke's Hospital, Hills Road, Cambridge CB2 OQQ, UK.
Susan E OzanneUniversity of Cambridge Metabolic Research Laboratories and MRC Metabolic Diseases Unit, Wellcome Trust-MRC Institute of Metabolic Science, Addenbrooke's Treatment Centre, Addenbrooke's Hospital, Hills Road, Cambridge CB2 OQQ, UK.
University of Cambridge · GBNational Hospital for Neurology and Neurosurgery · GB

Funding

British Heart Foundation FS/09/029/27902British Heart Foundation PG/09/037/27387Diabetes UK 12/0004508Medical Research Council MC_UU_12012/4
6 · The paper itself

Abstract

'Developmental programming', which occurs as a consequence of suboptimal in utero and early environments, can be associated with metabolic dysfunction in later life, including an increased incidence of cardiovascular disease and type 2 diabetes, and predisposition of older men to sarcopenia. However, the molecular mechanisms underpinning these associations are poorly understood. Many conditions associated with developmental programming are also known to be associated with the aging process. We therefore utilized our well-established rat model of low birth weight and accelerated postnatal catch-up growth (termed 'recuperated') in this study to establish the effects of suboptimal maternal nutrition on age-associated factors in skeletal muscle. We demonstrated accelerated telomere shortening (a robust marker of cellular aging) as evidenced by a reduced frequency of long telomeres (48.5-8.6 kb) and an increased frequency of short telomeres (4.2-1.3 kb) in vastus lateralis muscle from aged recuperated offspring compared to controls. This was associated with increased protein expression of the DNA-damage-repair marker 8-oxoguanine-glycosylase (OGG1) in recuperated offspring. Recuperated animals also demonstrated an oxidative stress phenotype, with decreased citrate synthase activity, increased electron-transport-complex activities of complex I, complex II-III and complex IV (all markers of functional mitochondria), and increased xanthine oxidase (XO), p67

Indexed as

Growth and DevelopmentMaternal Nutritional Physiological PhenomenaOxidative StressAgingAnimalsAntioxidantsBiomarkersDietDNA DamageFemaleInflammationMaleMuscle, SkeletalNF-kappa BOxidantsPhenotypeAntioxidantsBiomarkersNF-kappa BOxidantsDevelopmental programmingMitochondriaOxidative stressSkeletal muscle

Identifiers

PMID27585884
PMCPMC5087829
OpenAlexW2518651899

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.