Evidence map›Paper›PMID 15774527›Full record

ReviewThe Journal of physiology2005

Investigating the causes of low birth weight in contrasting ovine paradigms.

J M Wallace, T R H Regnault, S W Limesand, W W Hay, R V Anthony

Abstract readComparative StudyReview
In one paragraph

Review in The Journal of physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing 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

34 citing papers in PubMed.

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  16. A physiological increase in insulin suppresses gluconeogenic gene activation in fetal sheep with sustained hypoglycemia.American journal of physiology. Regulatory, integrative and comparative physiology · 2012
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors.

J M WallaceRowett Research Institute, Bucksburn, Aberdeen AB21 9SB, UK. jacqueline.wallace@rri.sari.ac.uk
T R H Regnault
S W Limesand
W W Hay
R V Anthony

Funding

Fetal pancreatic development &insulin secretionR01HD042815 · NICHD · UNIVERSITY OF COLORADO DENVER · PI HAY, WILLIAM W · 2002 to 2006
$2.7M
Fetoplacental amino acid metabolism in IUGR pregnanciesR01HD041505 · NICHD · UNIVERSITY OF COLORADO DENVER · PI WILKENING, RANDALL B · 2002 to 2006
$1.9M
FETAL GLUCOSE AND AMINO ACID DEPRIVATIONR01DK052138 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI HAY, WILLIAM W · 1997 to 2005
$1.9M
UMBILICAL VENOUS BLOOD FLOW &AMINOACID TRANSPORT &METABOLISMP01HD020761 · NICHD · UNIVERSITY OF COLORADO DENVER · PI BATTAGLIA, F · 1996 to 2000
$662k
SPONTANEOUS PLACENTAL INSUFFICIENCY--A MODEL OF FETAL GROWTH RETARDATIONP50HD020761 · NICHD · UNIVERSITY OF COLORADO DENVER · PI WILKENING, RANDALL B · 1985 to 1995
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NICHD NIH HHS HD20761NICHD NIH HHS HD41505NICHD NIH HHS HD42815NICHD NIH HHS R01 HD041505NICHD NIH HHS R01 HD042815NIDDK NIH HHS DK28794NIDDK NIH HHS DK52138NIDDK NIH HHS R01 DK052138
6 · The paper itself

Abstract

Intrauterine growth restriction (IUGR) still accounts for a large incidence of infant mortality and morbidity worldwide. Many of the circulatory and transport properties of the sheep placenta are similar to those of the human placenta and as such, the pregnant sheep offers an excellent model in which to study the development of IUGR. Two natural models of ovine IUGR are those of hyperthermic exposure during pregnancy, and adolescent overfeeding, also during pregnancy. Both models yield significantly reduced placental weights and an asymmetrically growth-restricted fetus, and display altered maternal hormone concentrations, indicative of an impaired trophoblast capacity. Additionally, impaired placental angiogenesis and uteroplacental blood flow appears to be an early defect in both the hyperthermic and adolescent paradigms. The effects of these alterations in placental functional development appear to be irreversible. IUGR fetuses are both hypoxic and hypoglycaemic, and have reduced insulin and insulin-like growth factor-1 (IGF-1), and elevated concentrations of lactate. However, fetal utilization of oxygen and glucose, on a weight basis, remain constant compared with control pregnancies. Maintained utilization of these substrates, in a substrate-deficient environment, suggests increased sensitivities to metabolic signals, which may play a role in the development of metabolic diseases in later adult life.

Indexed as

Disease Models, AnimalEnergy MetabolismInfant, Low Birth WeightPrenatal Exposure Delayed EffectsPrenatal Nutritional Physiological PhenomenaAnimalsAnimals, NewbornCardiovascular SystemDietFemaleFetal Growth RetardationHumansInfant, NewbornModels, AnimalModels, BiologicalPlacenta

Identifiers

PMID15774527
PMCPMC1464509

What OpenQuestion holds

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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.