Evidence map›Paper›PMID 22167521›Full record

ArticleAmerican journal of physiology. Endocrinology and metabolism2012

Hypoglycemia, hyperglucagonemia, and fetoplacental defects in glucagon receptor knockout mice: a role for glucagon action in pregnancy maintenance.

Sophia Ouhilal, Patricia Vuguin, Lingguang Cui, Xiu-Quan Du, Richard W Gelling, Sandra E Reznik, Robert Russell, Albert F Parlow, Clara Karpovsky, Nanette Santoro and 1 more

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Endocrinology and metabolism, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.9field-weighted citation impact, top 10% 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

25 citing papers in PubMed, 34 citations in OpenAlex.

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  6. The human α cell in health and disease.The Journal of endocrinology · 2023
    Review
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  20. Critical periods of increased fetal vulnerability to a maternal high fat diet.Reproductive biology and endocrinology : RB&E · 2014
    Article
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

11 authors at 6 institutions in 5 countries.

Sophia OuhilalDepartment of Obstetrics and Gynecology, Albert Einstein College of Medicine, Bronx, NY 10467, USA.
Patricia Vuguin
Lingguang Cui
Xiu-Quan Du
Richard W Gelling
Sandra E Reznik
Robert Russell
Albert F Parlow
Clara Karpovsky
Nanette Santoro
Maureen J Charron
Laboratoire de Biochimie · FRAlbert Einstein College of Medicine · USBeijing Obstetrics and Gynecology Hospital · CNAbbott (Singapore) · SGUCLA Medical Center · USUniversity of Colorado Denver · US

Funding

GLUT4 AND CARDIAC METABOLISM AND PHYSIOLOGYR01HL058119 · NHLBI · YESHIVA UNIVERSITY · PI CHARRON, MAUREEN J · 1997 to 2004
$1.5M
Nutrition, Early Development and Glucose MetabolismK08HD042172 · NICHD · MONTEFIORE MEDICAL CENTER (BRONX, NY) · PI VUGUIN, PATRICIA MYRIAM · 2003 to 2007
$634k
NHLBI NIH HHS HL-58119NICHD NIH HHS K08-HD-042172NIDDK NIH HHS DK-47435
6 · The paper itself

Abstract

Alterations in insulin signaling as well as insulin action predispose to infertility as well as adverse pregnancy outcomes; however, little is known about the role of glucagon signaling in reproduction. The glucagon receptor knockout (Gcgr(-/-)) mouse created by our laboratory was used to define the role of glucagon signaling in maintaining normal reproduction. In this mouse model, lack of glucagon signaling did not alter the hypothalamic-pituitary-ovarian axis. Pregnant Gcgr(-/-) female mice displayed persistent hypoglycemia and hyperglucagonemia. Gcgr(-/-) pregnancies were associated with decreased fetal weight, increased late-gestation fetal demise, and significant abnormalities of placentation. Gcgr(-/-) placentas contained areas of extensive mineralization, fibrinoid necrosis, narrowing of the vascular channels, and a thickened interstitium associated with trophoblast hyperplasia. Absent glucagon signaling did not alter glycogen content in Gcgr(-/-) placentas but significantly downregulated genes that control growth, adrenergic signaling, vascularization, oxidative stress, and G protein-coupled receptors. Our data suggest that, similarly to insulin, glucagon action contributes to normal female reproductive function.

Indexed as

AnimalsFemaleFetal DeathFetal DiseasesFetal Growth RetardationGene Expression Regulation, DevelopmentalGlucagonHeterozygoteHypoglycemiaMiceMice, Inbred C57BLMice, KnockoutOvaryPituitary Gland, AnteriorPlacentaPlacenta DiseasesGlucagonPregnancy ProteinsReceptors, Glucagon

Identifiers

PMID22167521
PMCPMC3311287
OpenAlexW2147422121

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.