Evidence map›Paper›PMID 23482706›Full record

ArticleThe Journal of endocrinology2013

Intrauterine growth restriction alters term fetal baboon hypothalamic appetitive peptide balance.

Cun Li, Thomas J McDonald, Guoyao Wu, Mark J Nijland, Peter W Nathanielsz

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of endocrinology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

38 citing papers in PubMed, 65 citations in OpenAlex.

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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

5 authors at 2 institutions in 1 country.

Cun LiDepartment of Obstetrics and Gynecology, Center for Pregnancy and Newborn Research, The University of Texas Health Science Center San Antonio, 7703 Floyd Curl Drive, San Antonio, Texas 78229, USA.
Thomas J McDonald
Guoyao Wu
Mark J Nijland
Peter W Nathanielsz
The University of Texas Health Science Center at San Antonio · USTexas A&M University · US

Funding

The Southwest National Primate Research Center Supplement- Infrastructure improvements of ABSL2 holding areasP51OD011133 · OD · TEXAS BIOMEDICAL RESEARCH INSTITUTE · PI Larry S. Schlesinger · 2012 to 2026
$129.7M
PARTURITION AND FETAL PRIMATE HYPOTHALAMIC FUNCTIONP01HD021350 · NICHD · UNIVERSITY OF WYOMING · PI NIJLAND, MARK J · 1987 to 2018
$19.9M
NICHD NIH HHS HD 21350NICHD NIH HHS P01 HD021350NIH HHS P51 OD011133
6 · The paper itself

Abstract

Neurons controlling appetite are located in the hypothalamic arcuate nuclei (ARH). Offspring appetite regulation has been shown to be modified by dysregulation of ARH nuclear development. Most ARH developmental studies have been in altricial rodents whose hypothalamic development is predominantly postnatal. In primates including humans, much development of hypothalamic appetite regulatory centers occurs before birth. We hypothesized that i) appetitive peptides are abundantly expressed by 90 percent gestation (0.9G), ready for postnatal function; ii) by 0.9G, intrauterine growth restriction (IUGR) increases the orexigenic:anorexigenic peptide ratio; iii) IUGR increases fetal glucocorticoid receptor (GR) expression; and iv) IUGR decreases STAT3, which signals inhibition of appetite. We developed a fetal baboon IUGR model resulting from reduced maternal nutrition. Pregnant baboons were fed ad libitum, controls (CTR; n=24), or 70% CTR diet to produce IUGR (n=14). C-section was performed at 0.9G. In CTR (n=7) and IUGR (n=6) fetal brains, ARH appetite regulatory peptides (neuropeptide Y (NPY) and proopiomelanocortin (POMC)) were quantified immunohistochemically. Fetal plasma cortisol was raised in IUGR fetuses. We observed that NPY and POMC were well expressed by 0.9G. IUGR increased NPY, GR, and active phosphorylated GR and decreased POMC and phosphorylated form of STAT3. We conclude that IUGR dysregulates ARH development in ways that will reset the appetitive neuropeptide balance in favor of increased appetite drive in postnatal life. We postulate that changes in peptide abundance are in part due to increased fetal cortisol and ARH GR. These changes may contribute to predisposition to obesity in IUGR offspring.

Indexed as

Maternal Nutritional Physiological PhenomenaAnimalsAppetite RegulationArcuate Nucleus of HypothalamusFemaleFetal Growth RetardationNeuropeptide YPapioPhosphorylationPregnancyPrenatal Exposure Delayed EffectsPro-OpiomelanocortinReceptors, GlucocorticoidSTAT3 Transcription FactorNeuropeptide YPro-OpiomelanocortinReceptors, GlucocorticoidSTAT3 Transcription Factor

Identifiers

PMID23482706
PMCPMC4018765
OpenAlexW2142015110

What OpenQuestion holds

Textmetadata
LicenceTDM
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.