Evidence map›Paper›PMID 23119079›Full record

ArticlePloS one2012

Adipocyte dysfunction in a mouse model of polycystic ovary syndrome (PCOS): evidence of adipocyte hypertrophy and tissue-specific inflammation.

Joseph S Marino, Jeffrey Iler, Abigail R Dowling, Streamson Chua, Jens C Bruning, Roberto Coppari, Jennifer W Hill

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 14% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

  1. Pooled it
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  6. Androgen-induced insulin resistance is ameliorated by deletion of hepatic androgen receptor in females.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
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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

7 authors at 4 institutions in 2 countries.

Joseph S MarinoDepartment of Physiology and Pharmacology, Center for Diabetes and Endocrine Research, University of Toledo Medical Center, Toledo, Ohio, United States of America.
Jeffrey Iler
Abigail R Dowling
Streamson Chua
Jens C Bruning
Roberto Coppari
Jennifer W Hill
University of Toledo Medical Center · USAlbert Einstein College of Medicine · USThe University of Texas Southwestern Medical Center · USUniversity of Cologne · DE

Funding

Regional Pilot And Feasibility Study Grants ProgramP30DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI DAVID P OLSON · 2013 to 2026
$24.3M
Mouse Phenotype Core, Project 9 of 10PL1DK081182 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI RUSSELL, DAVID W. · 2007 to 2011
$2.0M
Hypothalamic leptin and insulin signals aligning metabolic state and fertilityR00HD056491 · NICHD · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI HILL, JENNIFER WOOTTON · 2009 to 2011
$740k
Inflammatory triggers of polycystic ovarian syndrome.R21HD071529 · NICHD · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI HILL, JENNIFER WOOTTON · 2012 to 2013
$364k
Taskforce for Obesity Research at Southwestern (TORS)UL1RR024923 · NCRR · UT SOUTHWESTERN MEDICAL CENTER · PI HORTON, JAY D · 2007 to 2007
$235k
NCRR NIH HHS 1UL1RR024923NCRR NIH HHS UL1 RR024923NICHD NIH HHS R00 HD056491NICHD NIH HHS R00HD056491NICHD NIH HHS R21 HD071529NICHD NIH HHS R21HD071529NIDDK NIH HHS 1PL1DK081182NIDDK NIH HHS P30 DK020572NIDDK NIH HHS PL1 DK081182
6 · The paper itself

Abstract

Clinical research shows an association between polycystic ovary syndrome (PCOS) and chronic inflammation, a pathological state thought to contribute to insulin resistance. The underlying pathways, however, have not been defined. The purpose of this study was to characterize the inflammatory state of a novel mouse model of PCOS. Female mice lacking leptin and insulin receptors in pro-opiomelanocortin neurons (IR/LepR(POMC) mice) and littermate controls were evaluated for estrous cyclicity, ovarian and adipose tissue morphology, and body composition by QMR and CT scan. Tissue-specific macrophage infiltration and cytokine mRNA expression were measured, as well as circulating cytokine levels. Finally, glucose regulation during pregnancy was evaluated as a measure of risk for diabetes development. Forty-five percent of IR/LepR(POMC) mice showed reduced or absent ovulation. IR/LepR(POMC) mice also had increased fat mass and adipocyte hypertrophy. These traits accompanied elevations in macrophage accumulation and inflammatory cytokine production in perigonadal adipose tissue, liver, and ovary. These mice also exhibited gestational hyperglycemia as predicted. This report is the first to show the presence of inflammation in IR/LepR(POMC) mice, which develop a PCOS-like phenotype. Thus, IR/LepR(POMC) mice may serve as a new mouse model to clarify the involvement of adipose and liver tissue in the pathogenesis and etiology of PCOS, allowing more targeted research on the development of PCOS and potential therapeutic interventions.

Indexed as

Disease Models, AnimalAdipocytesAdipose TissueAnimalsBlood GlucoseFemaleGene ExpressionHumansHypertrophyInflammationInterleukin-1betaInterleukin-6LiverMagnetic Resonance ImagingMaleMiceBlood GlucoseInterleukin-1betaInterleukin-6Receptor, InsulinReceptors, Leptin

Identifiers

PMID23119079
PMCPMC3485364
OpenAlexW2157689564

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.