Evidence map›Paper›PMID 32382742›Full record

ArticleThe Journal of clinical endocrinology and metabolism2020

Adipocyte Insulin Resistance in PCOS: Relationship With GLUT-4 Expression and Whole-Body Glucose Disposal and β-Cell Function.

Uche Ezeh, Ida Y-D Chen, Yen-Hao Chen, Ricardo Azziz

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical endocrinology and metabolism, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 9% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

  1. Adipose Tissue Dysfunction in Polycystic Ovary Syndrome.The Journal of clinical endocrinology and metabolism · 2023
    Pooled it
  2. Review
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  9. Polycystic ovary syndrome as a metabolic disease.Nature reviews. Endocrinology · 2025
    Review
  10. Shared Pathophysiological Mechanisms and Genetic Factors in Early Menarche and Polycystic Ovary Syndrome.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Review
  11. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Uche EzehDepartment of Obstetrics and Gynecology, Stanford Healthcare-ValleyCare Hospital, Pleasanton, California.
Ida Y-D ChenDepartment of Obstetrics & Gynecology and Center for Androgen-Related Disorders, Cedars-Sinai Medical Center, Los Angeles, California.
Yen-Hao ChenDepartment of Obstetrics & Gynecology and Center for Androgen-Related Disorders, Cedars-Sinai Medical Center, Los Angeles, California.
Ricardo AzzizDepartment of Obstetrics & Gynecology and Center for Androgen-Related Disorders, Cedars-Sinai Medical Center, Los Angeles, California.
Cedars-Sinai Medical Center · US

Funding

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
NICHD NIH HHS K24 HD001346NICHD NIH HHS R01 HD029364NIDDK NIH HHS R01 DK073632
6 · The paper itself

Abstract

contextImpaired sensitivity to the antilipolytic action of insulin in adipose tissue (AT) may play a role in determining metabolic dysfunction in polycystic ovary syndrome (PCOS).

objectivesTo test the hypothesis that insulin resistance (IR) in AT is associated with whole-body insulin sensitivity and β-cell function in PCOS. RESEARCH DESIGN AND

settingProspective cross-sectional study.

methodsEighteen participants with PCOS and 18-matched control participants underwent a modified frequently sampled intravenous glucose tolerance test (mFSIVGTT); subgroups underwent single-slice computed tomography scans determining AT distribution and adipocyte glucose transporter type 4 (GLUT-4) expression.

main outcome measuresIR in AT in basal (by the adipose insulin resistance index [Adipo-IR]) and dynamic (mFSIVGTT-derived indices of insulin-mediated nonesterified fatty acids [NEFA] suppression [NEFAnadir, TIMEnadir, and %NEFAsupp]) states; whole-body insulin-mediated glucose uptake and insulin secretion in basal (by homeostatic model assessment [HOMA]-IR and HOMA-β%) and dynamic (mFSIVGTT-derived insulin sensitivity index [Si], acute insulin response to glucose [AIRg], and disposition index [Di]) states.

resultsParticipants with PCOS had higher HOMA-IR and HOMA-β%, lower Si and Di, higher longer TIMEnadir, higher Adipo-IR and NEFAnadir, and a trend toward lower GLUT-4, than the control group participants. Adipo-IR was associated with dynamic state IR in AT (NEFAnadir TIMEnadir, and %NEFAsupp), but only in PCOS, and with HOMA-IR and HOMA-β% in both groups. NEFAnadir and TIMEnadir were negatively and %NEFAsupp positively associated with Si only in PCOS, but not with AIRg and Di, or GLUT-4 expression.

conclusionWomen with PCOS demonstrated increased IR in AT, which is closely associated with whole-body IR but not with dynamic state β-cell function or adipocyte GLUT-4 gene expression.

Indexed as

AdipocytesAdultBlood GlucoseCross-Sectional StudiesFemaleGene ExpressionGlucose Tolerance TestGlucose Transporter Type 4HumansInsulinInsulin ResistanceInsulin SecretionPolycystic Ovary SyndromeProspective StudiesBlood GlucoseGlucose Transporter Type 4InsulinSLC2A4 protein, humanAdipocytefatty acidsGLUT-4insulin resistancePCOSβ-cell function

Identifiers

PMID32382742
PMCPMC7274487
OpenAlexW3020881133

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.