Evidence map›Paper›PMID 22904174›Full record

ArticleThe Journal of clinical endocrinology and metabolism2012

Inflammation in response to glucose ingestion is independent of excess abdominal adiposity in normal-weight women with polycystic ovary syndrome.

Frank González, Chang Ling Sia, Marguerite K Shepard, Neal S Rote, Judi Minium

Open access · greenAbstract read
In one paragraph

Article in The Journal of clinical endocrinology and metabolism, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 2 pooled it
4.1field-weighted citation impact, top 7% 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

25 citing papers in PubMed, 2 syntheses or guidelines pooled it, 44 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. On the Intimate Relationship of Adiposity to Polycystic Ovary Syndrome.The Journal of clinical endocrinology and metabolism · 2025
    Review
  5. Review
  6. Saturated fat ingestion stimulates proatherogenic inflammation in polycystic ovary syndrome.American journal of physiology. Endocrinology and metabolism · 2021
    Article
  7. Review
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  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Is Afamin a novel biomarker for gestational diabetes mellitus? A pilot study.Reproductive biology and endocrinology : RB&E · 2018
    Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article
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

5 authors at 3 institutions in 1 country.

Frank GonzálezIndiana University School of Medicine, Department of Obstetrics and Gynecology, AOC Room 6046, 550 North University Boulevard, Indianapolis, Indiana 46202, USA. gonzalef@iupui.edu
Chang Ling Sia
Marguerite K Shepard
Neal S Rote
Judi Minium
Indiana University – Purdue University Indianapolis · USCase Western Reserve University · USUniversity School · 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

contextInflammation and excess abdominal adiposity (AA) are often present in normal-weight women with polycystic ovary syndrome (PCOS).

objectiveWe determined the effects of hyperglycemia on nuclear factor-κB (NFκB) activation in mononuclear cells (MNC) of normal-weight women with PCOS with and without excess AA.

designThis was a prospective controlled study.

settingThe study was conducted at an academic medical center. PATIENTS: Fifteen normal-weight, reproductive-age women with PCOS (seven normal AA, eight excess AA) and 16 body composition-matched controls (eight normal AA, eight excess AA) participated in the study.

main outcome measuresBody composition was measured by dual-energy absorptiometry. Insulin sensitivity was derived from an oral glucose tolerance test (IS(OGTT)). Activated NFκB and the protein content of p65 and inhibitory-κB were quantified from MNC, and TNFα and C-reactive protein (CRP) were measured in plasma obtained from blood drawn while fasting and 2 h after glucose ingestion.

resultsCompared with controls, both PCOS groups exhibited lower IS(OGTT), increases in activated NFκB and p65 protein, and decreases in inhibitory-κB protein. Compared with women with PCOS with excess AA, those with normal AA exhibited higher testosterone levels and lower TNFα and CRP levels. For the combined groups, the percent change in NFκB activation was negatively correlated with IS(OGTT) and positively correlated with androgens. TNFα and CRP were positively correlated with abdominal fat.

conclusionIn normal-weight women with PCOS, the inflammatory response to glucose ingestion is independent of excess AA. Circulating MNC and excess AA are separate and unique sources of inflammation in this population.

Indexed as

Abdominal FatAdiposityAdultBiomarkersC-Reactive ProteinFemaleGlucoseGlucose Tolerance TestHumansHyperglycemiaInflammationInsulin ResistanceLeukocytes, MononuclearNF-kappa BPolycystic Ovary SyndromeProspective StudiesBiomarkersC-Reactive ProteinGlucoseNF-kappa BTumor Necrosis Factor-alpha

Identifiers

PMID22904174
PMCPMC3485595
OpenAlexW2051737682

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.