Evidence map›Paper›PMID 22178787›Full record

ReviewSteroids2012

Inflammation in Polycystic Ovary Syndrome: underpinning of insulin resistance and ovarian dysfunction.

Frank González

Registry-linked trialOpen access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Steroids, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06567132 (Evaluation of the Effect of Non-Surgical Periodontal Treatment on IL-6, IL-10 and ANXA-1 Levels in Women With Polycystic Ovary Syndrome), which is not on this map. Cited by 255 papers, 13 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
255citing papers in PubMed, 13 pooled it
12.2field-weighted citation impact, top 1% 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.

NCT06567132 nacompletednot on this mapstarted 2022, after this paper: background citation

Evaluation of the Effect of Non-Surgical Periodontal Treatment on IL-6, IL-10 and ANXA-1 Levels in Women With Polycystic Ovary Syndrome

TypeinterventionalSponsorBezmialem Vakif UniversityRan2022 to 2023Enrolled80ConditionsPolycystic Ovary Syndrome, GingivitisArmsNon-surgical periodontal treatment
3 · Its place in the literature

Who cites it

255 citing papers in PubMed, 13 syntheses or guidelines pooled it, 471 citations in OpenAlex.

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  9. Curcumin and Polycystic Ovary Syndrome: a Systematic Review.Reproductive sciences (Thousand Oaks, Calif.) · 2022
    Pooled it
  10. Gut Microbiota in Patients with Polycystic Ovary Syndrome: a Systematic Review.Reproductive sciences (Thousand Oaks, Calif.) · 2022
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195 more citing papers are in PubMed but not listed here.

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

1 author at 1 institution in 1 country.

Frank GonzálezIndiana University School of Medicine, Department of Obstetrics and Gynecology, Division of Reproductive Endocrinology and Infertility, Indianapolis, IN 46202, USA. gonzalef@iupui.edu
Indiana University – Purdue University Indianapolis · US

Funding

Inflammation: Effect on Insulin Resistance in PCOSR03HD048535 · NICHD · MAYO CLINIC ROCHESTER · PI GONZALEZ, FRANK · 2006 to 2007
$146k
NICHD NIH HHS HD-048535NICHD NIH HHS R03 HD048535
6 · The paper itself

Abstract

Chronic low-grade inflammation has emerged as a key contributor to the pathogenesis of Polycystic Ovary Syndrome (PCOS). A dietary trigger such as glucose is capable of inciting oxidative stress and an inflammatory response from mononuclear cells (MNC) of women with PCOS, and this phenomenon is independent of obesity. This is important because MNC-derived macrophages are the primary source of cytokine production in excess adipose tissue, and also promote adipocyte cytokine production in a paracrine fashion. The proinflammatory cytokine tumor necrosis factor-α (TNFα) is a known mediator of insulin resistance. Glucose-stimulated TNFα release from MNC along with molecular markers of inflammation are associated with insulin resistance in PCOS. Hyperandrogenism is capable of activating MNC in the fasting state, thereby increasing MNC sensitivity to glucose; and this may be a potential mechanism for promoting diet-induced inflammation in PCOS. Increased abdominal adiposity is prevalent across all weight classes in PCOS, and this inflamed adipose tissue contributes to the inflammatory load in the disorder. Nevertheless, glucose ingestion incites oxidative stress in normal weight women with PCOS even in the absence of increased abdominal adiposity. In PCOS, markers of oxidative stress and inflammation are highly correlated with circulating androgens. Chronic suppression of ovarian androgen production does not ameliorate inflammation in normal weight women with the disorder. Furthermore, in vitro studies have demonstrated the ability of pro-inflammatory stimuli to upregulate the ovarian theca cell steroidogenic enzyme responsible for androgen production. These findings support the contention that inflammation directly stimulates the polycystic ovary to produce androgens.

Indexed as

Insulin ResistanceAnimalsDietFemaleHumansInflammationOvaryPolycystic Ovary Syndrome

Identifiers

PMID22178787
PMCPMC3309040
OpenAlexW2042639777

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.