Evidence map›Paper›PMID 18178198›Full record

ArticleFertility and sterility2008

Adipocytes from women with polycystic ovary syndrome demonstrate altered phosphorylation and activity of glycogen synthase kinase 3.

Wendy Chang, Mark O Goodarzi, Heith Williams, Denis A Magoffin, Marita Pall, Ricardo Azziz

Open access · bronzeAbstract read
In one paragraph

Article in Fertility and sterility, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 12% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. Adipose Tissue Dysfunction in Polycystic Ovary Syndrome.The Journal of clinical endocrinology and metabolism · 2023
    Pooled it
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  11. Adipose Insulin Resistance in Normal-Weight Women With Polycystic Ovary Syndrome.The Journal of clinical endocrinology and metabolism · 2019
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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

6 authors at 1 institution in 1 country.

Wendy ChangDepartment of Obstetrics and Gynecology, Division of Endocrinology, Diabetes and Metabolism, Cedars-Sinai Medical Center, Los Angeles, California 90048, USA.
Mark O Goodarzi
Heith Williams
Denis A Magoffin
Marita Pall
Ricardo Azziz
Cedars-Sinai Medical Center · US

Funding

ZONA-FREE HAMSTER OVA ASSAY AS AN INDICATOR OF MALE FERTILITYM01RR000425 · NCRR · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · PI ANDERSON, GAIL V · 1985 to 2011
$74.2M
ADRENAL ANDROGEN EXCESS IN THE POLYCYSTIC OVARY SYNDROMER01HD029364 · NICHD · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI AZZIZ, RICARDO · 1993 to 2011
$2.2M
INSULIN SIGNALING DEFECTS IN PCOSR01DK073632 · NIDDK · CEDARS-SINAI MEDICAL CENTER · PI AZZIZ, RICARDO · 2006 to 2010
$1.9M
ANDROGEN EXCESS DISORDERK24HD001346 · NICHD · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI AZZIZ, RICARDO · 2000 to 2004
$455k
Molecular Defects of Insulin Signaling in PCOSR03HD042077 · NICHD · CEDARS-SINAI MEDICAL CENTER · PI AZZIZ, RICARDO · 2003 to 2004
$153k
NCRR NIH HHS M01 RR000425NCRR NIH HHS M01-RR00425NICHD NIH HHS 03-HD42077NICHD NIH HHS K24 HD001346NICHD NIH HHS K24-HD01346-01NICHD NIH HHS R01 HD029364NICHD NIH HHS R01-HD29364NICHD NIH HHS R03 HD042077NIDDK NIH HHS R01 DK073632
6 · The paper itself

Abstract

objectiveTo test the hypothesis that an abnormality in glycogen synthase kinase-3 (GSK3) is a pathogenic factor in polycystic ovary syndrome (PCOS).

designProspective experimental study (adipocytes).

settingTertiary-care academic medical center and teaching hospital. PATIENT(S): Twenty patients with PCOS and 21 healthy control women. INTERVENTION(S): Blood sampling, physical exam, biopsy of SC lower abdominal fat. MAIN OUTCOME MEASURE(S): Glucose transport and protein levels and phosphorylation state of glycogen synthase kinase (GSK)-3alpha and GSK3beta in adipocytes; assessment of GSK3beta activity. RESULT(S): Basal protein levels of glycogen synthase kinase (GSK3alpha and GSK3beta) did not differ between control women and women with PCOS, nor did basal or insulin-stimulated levels of serine phosphorylated GSK3alpha. However, in adipocytes of women with PCOS, insulin stimulation was not associated with increased serine phosphorylation of GSK3beta, in contrast to the case of control women. Tyrosine phosphorylation of GSK3beta also was higher in women with PCOS, compared with in control women. Consistent with the phosphorylation data, GSK3beta activity was elevated in PCOS adipocytes. CONCLUSION(S): These data suggest that GSK3beta is hyperactivated and resistant to down-regulation by insulin in PCOS. By using physiologic approaches, we demonstrated that abnormal GSK3beta regulation is a potential mechanism for the insulin resistance that is seen in some women with PCOS, which may contribute to their development of the syndrome.

Indexed as

Insulin Resistance3-O-MethylglucoseAdipocytesAdultCase-Control StudiesFemaleGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHumansInsulinMiddle AgedPhosphorylationPolycystic Ovary SyndromeProspective StudiesYoung Adult3-O-MethylglucoseGlycogen Synthase Kinase 3glycogen synthase kinase 3 alphaGlycogen Synthase Kinase 3 betaGSK3B protein, humanInsulin

Identifiers

PMID18178198
PMCPMC2744855
OpenAlexW2144261298

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.