CoChat
Sign Up
Cited by 123Ovarian function and disordersAdipokines, Inflammation, and Metabolic DiseasesCardiovascular Disease and Adiposity

The DOI matches its Crossref record; 152 of the 156 references it cites were found in a registry or an index.

Adipose Tissue Dysfunction in Polycystic Ovary Syndrome

Open access
Bril, Fernando, Ezeh, Uche, Amiri, Mina, Hatoum, Sana, Pace, Lauren, Chen, Yen-Hao, Bertrand, Fred, Gower, Barbara, Azziz, Ricardo·2023·The Journal of Clinical Endocrinology & Metabolism
DOI 10.1210/clinem/dgad356PMC PMC10735305
Open this paper in CoChat — free accountOpen PDF

Abstract

Purpose: Polycystic ovary syndrome (PCOS) is a complex genetic trait and the most common endocrine disorder of women, clinically evident in 5% to 15% of reproductive-aged women globally, with associated cardiometabolic dysfunction. Adipose tissue (AT) dysfunction appears to play an important role in the pathophysiology of PCOS even in patients who do not have excess adiposity. Methods: We undertook a systematic review concerning AT dysfunction in PCOS, and prioritized studies that assessed AT function directly. We also explored therapies that targeted AT dysfunction for the treatment of PCOS. Results: Various mechanisms of AT dysfunction in PCOS were identified including dysregulation in storage capacity, hypoxia, and hyperplasia; impaired adipogenesis; impaired insulin signaling and glucose transport; dysregulated lipolysis and nonesterified free fatty acids (NEFAs) kinetics; adipokine and cytokine dysregulation and subacute inflammation; epigenetic dysregulation; and mitochondrial dysfunction and endoplasmic reticulum and oxidative stress. Decreased glucose transporter-4 expression and content in adipocytes, leading to decreased insulin-mediated glucose transport in AT, was a consistent abnormality despite no alterations in insulin binding or in IRS/PI3K/Akt signaling. Adiponectin secretion in response to cytokines/chemokines is affected in PCOS compared to controls. Interestingly, epigenetic modulation via DNA methylation and microRNA regulation appears to be important mechanisms underlying AT dysfunction in PCOS. Conclusion: AT dysfunction, more than AT distribution and excess adiposity, contributes to the metabolic and inflammation abnormalities of PCOS. Nonetheless, many studies provided contradictory, unclear, or limited data, highlighting the urgent need for additional research in this important field.

Overview

Integrity signals

Registry

Crossref · 10.1210/clinem/dgad356

Cites

152 of 152 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Verification

Claims the paper makes

We couldn’t retrieve this paper’s full text, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Citations

Cites

Show all 156 references

Cited by

Sorted by citations

See all 123

Related

Metadata

Authors
Bril, F., Ezeh, U., Amiri, M., Hatoum, S., Pace, L., Chen, Y.-H., Bertrand, F., Gower, B., & Azziz, R.
Affiliations
  • University of Alabama at Birmingham (US)
  • Research Institute for Endocrine Sciences (IR)
  • Foundation for Research and Education Excellence , Vestavia, AL 35243 , USA
  • Department of Research, Biomere-West , Richmond, CA 94806 , USA
Corresponding author
Azziz, Ricardo
ORCID
Venue
The Journal of Clinical Endocrinology & Metabolism
Publisher
The Endocrine Society
Published
2023-06-17
Volume
109
Issue
1
Pages
10-24
ISSN
  • 0021-972X (ISSN-L)
  • 1945-7197
DOI
10.1210/clinem/dgad356
PMC
PMC10735305
OpenAlex
W4381047110
Cited by
123
References
156
Citations by year
2026: 54 · 2025: 43 · 2024: 22 · 2023: 3
FWCI
4.95
Type
journal article
Language
en
Open access
Licence
academic.oup.com/pages/standard-publication-reuse-rights (vor)
Locations
  • The Journal of Clinical Endocrinology & Metabolism (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (1-K24-HD01346, R01-DK073632, R01-HD29364))
  • Helping Hand of Los Angeles, Inc
  • Research and Education Excellence
Topics
  • Health Sciences › Medicine › Reproductive Medicine › Ovarian function and disorders
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Disease and Adiposity
Keywords
polycystic ovary syndrome, adipose tissue dysfunction, insulin resistance, glucose transport, glucose transporter 4, adiponectin, adipokines, inflammation, epigenetic regulation, DNA methylation, microRNA, mitochondrial dysfunction, oxidative stress, endoplasmic reticulum stress, lipolysis, free fatty acids, adipocyte hyperplasia, adipogenesis, cardiometabolic dysfunction
MeSH terms
Adipose Tissue, Adult, Female, Glucose, Humans, Inflammation, Insulin, Insulin Resistance, Obesity, Polycystic Ovary Syndrome, Cytokines, Phosphatidylinositol 3-Kinases

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review