Evidence map›Paper›PMID 19605766›Full record

ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2009

Maternal obesity accelerates fetal pancreatic beta-cell but not alpha-cell development in sheep: prenatal consequences.

Stephen P Ford, Liren Zhang, Meijun Zhu, Myrna M Miller, Derek T Smith, Bret W Hess, Gary E Moss, Peter W Nathanielsz, Mark J Nijland

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed, 3 pooled it
19.6field-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

89 citing papers in PubMed, 3 syntheses or guidelines pooled it, 173 citations in OpenAlex.

  1. Pooled it
  2. Maternal obesity in pregnancy impacts offspring cardiometabolic health: Systematic review and meta-analysis of animal studies.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2019
    Pooled it
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  16. Large animal models in the study of gynecological diseases.Frontiers in cell and developmental biology · 2023
    Review
  17. Role of Obesity in Female Reproduction.International journal of medical sciences · 2023
    Review
  18. Review
  19. Review
  20. Article

29 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Stephen P FordCenter for the Study of Fetal Programming, Department of Animal Science, University of Wyoming, Laramie, Wyoming, USA.
Liren Zhang
Meijun Zhu
Myrna M Miller
Derek T Smith
Bret W Hess
Gary E Moss
Peter W Nathanielsz
Mark J Nijland
University of Wyoming · US

Funding

Wyoming IDeA Networks of Biomedical Research ExcellenceP20RR016474 · NCRR · UNIVERSITY OF WYOMING · PI LIBERLES, DAVID A. · 2001 to 2011
$28.2M
PARTURITION AND FETAL PRIMATE HYPOTHALAMIC FUNCTIONP01HD021350 · NICHD · UNIVERSITY OF WYOMING · PI NIJLAND, MARK J · 1987 to 2018
$19.9M
NCRR NIH HHS P20-RR-16474-04NICHD NIH HHS HD-21350NICHD NIH HHS P01 HD021350
6 · The paper itself

Abstract

Maternal obesity affects offspring weight, body composition, and organ function, increasing diabetes and metabolic syndrome risk. We determined effects of maternal obesity and a high-energy diet on fetal pancreatic development. Sixty days prior to breeding, ewes were assigned to control [100% of National Research Council (NRC) recommendations] or obesogenic (OB; 150% NRC) diets. At 75 days gestation, OB ewes exhibited elevated insulin-to-glucose ratios at rest and during a glucose tolerance test, demonstrating insulin resistance compared with control ewes. In fetal studies, ewes ate their respective diets from 60 days before to 75 days after conception when animals were euthanized under general anesthesia. OB and control ewes increased in body weight by approximately 43% and approximately 6%, respectively, from diet initiation until necropsy. Although all organs were heavier in fetuses from OB ewes, only pancreatic weight increased as a percentage of fetal weight. Blood glucose, insulin, and cortisol were elevated in OB ewes and fetuses on day 75. Insulin-positive cells per unit pancreatic area were 50% greater in fetuses from OB ewes as a result of increased beta-cell mitoses rather than decreased programmed cell death. Lambs of OB ewes were born earlier but weighed the same as control lambs; however, their crown-to-rump length was reduced, and their fat mass was increased. We conclude that increased systemic insulin in fetuses from OB ewes results from increased glucose exposure and/or cortisol-induced accelerated fetal beta-cell maturation and may contribute to premature beta-cell function loss and predisposition to obesity and metabolic disease in offspring.

Indexed as

Insulin ResistanceMaternal Nutritional Physiological PhenomenaAnimalsAnimals, NewbornBlood GlucoseCell ProliferationDisease Models, AnimalFemaleFetal DevelopmentFetusGestational AgeGlucagon-Secreting CellsHydrocortisoneInsulinInsulin-Secreting CellsMitosisBlood GlucoseHydrocortisoneInsulin

Identifiers

PMID19605766
PMCPMC2739779
OpenAlexW2400971304

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.