Evidence map›Paper›PMID 24512496›Full record

Trial reportThe Journal of clinical endocrinology and metabolism2014

Hyperandrogenism induces a proinflammatory TNFα response to glucose ingestion in a receptor-dependent fashion.

Frank González, Chang Ling Sia, Dawn M Bearson, Hilary E Blair

Registry-linked trialOpen access · bronzeAbstract readRandomized Controlled Trial
In one paragraph

Trial report in The Journal of clinical endocrinology and metabolism, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07490964 (Pathogenesis of Functional Hyperandrogenism in Women With Type 1 Diabetes Mellitus), which is not on this map. Cited by 27 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 4 pooled it
4.4field-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.

NCT07490964 not yet recruitingnot on this mapstarted 2026, after this paper: background citation

Pathogenesis of Functional Hyperandrogenism in Women With Type 1 Diabetes Mellitus: From Genetic-molecular Mechanisms to Clinical Phenotype.

TypeobservationalSponsorFundacion para la Investigacion Biomedica del Hospital Universitario Ramon y CajalRan2026 to 2028Enrolled60ConditionsType 1 Diabetes Mellitus, Polycystic Ovary Syndrome (PCOS)ArmsType 1 diabetes mellitus, Elevated circulating androgen levels, Sex dimorphism
3 · Its place in the literature

Who cites it

27 citing papers in PubMed, 4 syntheses or guidelines pooled it, 49 citations in OpenAlex.

  1. Adipose Tissue Dysfunction in Polycystic Ovary Syndrome.The Journal of clinical endocrinology and metabolism · 2023
    Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Trial
  6. Trial
  7. Review
  8. Article
  9. Protective Effects ofJournal of pharmacopuncture · 2024
    Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Characterizing skeletal muscle dysfunction in women with polycystic ovary syndrome.Therapeutic advances in endocrinology and metabolism · 2022
    Review
  17. Article
  18. Article
  19. Article
  20. Elevated ovarian pentraxin 3 in polycystic ovary syndrome.Journal of assisted reproduction and genetics · 2021
    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

4 authors at 3 institutions in 1 country.

Frank GonzálezDepartment of Obstetrics and Gynecology (F.G., C.L.S.), Indiana University School of Medicine, Indianapolis, Indiana 46202; and Department of Laboratory Medicine and Pathology (D.M.B., H.E.B.), College of Medicine, Mayo Clinic, Rochester, Minnesota 55905.
Chang Ling Sia
Dawn M Bearson
Hilary E Blair
Mayo Clinic · USIndiana University – Purdue University Indianapolis · USIndiana University School of Medicine

Funding

Mayo Clinic Center for Translational Science ActivitiesUL1TR000135 · NCATS · MAYO CLINIC ROCHESTER · PI KHOSLA, SUNDEEP · 2012 to 2015
$41.2M
Inflammation: Effect on Insulin Resistance in PCOSR03HD048535 · NICHD · MAYO CLINIC ROCHESTER · PI GONZALEZ, FRANK · 2006 to 2007
$146k
NCATS NIH HHS UL1 TR000135NCATS NIH HHS UL1TR000135NICHD NIH HHS HD-048535NICHD NIH HHS R03 HD048535
6 · The paper itself

Abstract

contextHyperandrogenism and inflammation are related in polycystic ovary syndrome (PCOS). Hyperandrogenemia can induce inflammation in reproductive-age women, but the mechanism for this phenomenon is unclear.

objectiveWe examined the in vivo and in vitro effects of hyperandrogenism on mononuclear cell (MNC)-derived androgen receptor (AR) status and TNFα release.

designThis study combined a randomized, controlled, double-blind protocol with laboratory-based cell culture experiments.

settingThis work was performed in an academic medical center.

participantsLean, healthy, reproductive-age women were treated with 130 mg of dehydroepiandrosterone (DHEA) or placebo (n = 8 subjects each) for 5 days and also provided untreated fasting blood samples (n = 12 subjects) for cell culture experiments.

main outcome measuresAR mRNA content and TNFα release were measured before and after DHEA administration in the fasting state and 2 hours after glucose ingestion. TNFα release in the fasting state was also measured in cultured MNCs exposed to androgens with or without flutamide preincubation.

resultsAt baseline, subjects receiving DHEA or placebo exhibited no significant difference in androgens and TNFα release from MNCs before and after glucose ingestion. Compared with placebo, DHEA administration raised levels of T, androstenedione, and DHEA sulfate, and increased MNC-derived AR mRNA content and TNFα release in the fasting state and in response to glucose ingestion. Compared with MNC exposure to baseline concentrations of DHEA (175 ng/dL) or T (50 ng/dL), the absolute change in TNFα release increased after exposure to T concentrations of 125 and 250 ng/dL and a DHEA concentration of 1750 ng/dL. Preincubation with flutamide reduced the TNFα response by ≥ 60% across all T concentrations.

conclusionAndrogen excess in vivo and in vitro comparable to what is present in PCOS increases TNFα release from MNCs of lean healthy reproductive-age women in a receptor-dependent fashion. Hyperandrogenemia activates and sensitizes MNCs to glucose in this population.

Indexed as

AdultAndrostenedioneDehydroepiandrosteroneDehydroepiandrosterone SulfateDouble-Blind MethodFemaleGlucoseHumansHyperandrogenismInflammationLeukocytes, MononuclearReceptors, AndrogenTestosteroneTumor Necrosis Factor-alphaAndrostenedioneDehydroepiandrosteroneDehydroepiandrosterone SulfateGlucoseReceptors, AndrogenTestosteroneTumor Necrosis Factor-alpha

Identifiers

PMID24512496
PMCPMC4010708
OpenAlexW2013885669

What OpenQuestion holds

Textmetadata
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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.