Evidence map›Paper›PMID 21045167›Full record

ArticleReproduction (Cambridge, England)2011

Suboptimal maternal nutrition, during early fetal liver development, promotes lipid accumulation in the liver of obese offspring.

M A Hyatt, D S Gardner, S Sebert, V Wilson, N Davidson, Y Nigmatullina, L L Y Chan, H Budge, M E Symonds

Open access · hybridAbstract read
In one paragraph

Article in Reproduction (Cambridge, England), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
5.5field-weighted citation impact, top 5% 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

19 citing papers in PubMed, 60 citations in OpenAlex.

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  12. Developmental origins of NAFLD: a womb with a clue.Nature reviews. Gastroenterology & hepatology · 2017
    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

9 authors at 2 institutions in 1 country.

M A HyattEarly Life Nutrition Research Unit, Academic Child Health Respiratory Biomedical Research Unit, School of Clinical Sciences, Queen's Medical Centre, University Hospital, Nottingham, UK.
D S Gardner
S Sebert
V Wilson
N Davidson
Y Nigmatullina
L L Y Chan
H Budge
M E Symonds
University of Nottingham · GBQueen's Medical Centre · GB

Funding

British Heart FoundationWellcome Trust
6 · The paper itself

Abstract

Maternal nutrition during the period of early organ development can modulate the offspring's ability to metabolise excess fat as young adults when exposed to an obesogenic environment. This study examined the hypothesis that exposing offspring to nutrient restriction coincident with early hepatogenesis would result in endocrine and metabolic adaptations that subsequently lead to increased ectopic lipid accumulation within the liver. Pregnant sheep were fed either 50 or 100% of total metabolisable energy requirements from 30 to 80 days gestation and 100% thereafter. At weaning, offspring were made obese, and at ~1 year of age livers were sampled. Lipid infiltration and molecular indices of gluconeogenesis, lipid metabolism and mitochondrial function were measured. Although hepatic triglyceride accumulation was not affected by obesity per se, it was nearly doubled in obese offspring born to nutrient-restricted mothers. This adaptation was accompanied by elevated gene expression for peroxisome proliferator-activated receptor γ (PPARG) and its co-activator PGC1α, which may be indicative of changes in the rate of hepatic fatty acid oxidation. In contrast, maternal diet had no influence on the stimulatory effect of obesity on gene expression for a range of proteins involved in glucose metabolism and energy balance including glucokinase, glucocorticoid receptors and uncoupling protein 2. Similarly, although gene expressions for the insulin and IGF1 receptors were suppressed by obesity they were not influenced by the prenatal nutritional environment. In conclusion, excess hepatic lipid accumulation with juvenile obesity is promoted by suboptimal nutrition coincident with early development of the fetal liver.

Indexed as

Animal Nutritional Physiological PhenomenaMaternal Nutritional Physiological PhenomenaPrenatal Exposure Delayed EffectsAge FactorsAnimalsDisease Models, AnimalFatty LiverFemaleGene Expression Regulation, DevelopmentalGestational AgeGluconeogenesisLipid MetabolismLiverMalnutritionMitochondria, LiverObesityPPAR gammaTriglycerides

Identifiers

PMID21045167
PMCPMC3001618
OpenAlexW1974519034

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.