Evidence map›Paper›PMID 17445549›Full record

ArticleMetabolism: clinical and experimental2007

The adipose cell lineage is not intrinsically insulin resistant in polycystic ovary syndrome.

Anne Corbould, Andrea Dunaif

Open access · greenAbstract read
In one paragraph

Article in Metabolism: clinical and experimental, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
5.3field-weighted citation impact, top 5% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

  1. Pooled it
  2. On the Intimate Relationship of Adiposity to Polycystic Ovary Syndrome.The Journal of clinical endocrinology and metabolism · 2025
    Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Endocrine causes of nonalcoholic fatty liver disease.World journal of gastroenterology · 2015
    Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Sheep models of polycystic ovary syndrome phenotype.Molecular and cellular endocrinology · 2013
    Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  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

2 authors at 2 institutions in 1 country.

Anne CorbouldDivision of Women's Health, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. anne.corbould@princehenrys.org
Andrea Dunaif
Brigham and Women's Hospital · USHarvard University · US

Funding

Zoledronic Acid in Treatment of Osteoporosis in PostmenoM01RR002635 · NCRR · BRIGHAM AND WOMEN'S HOSPITAL · PI GARBER, JUDY E. · 1985 to 2008
$48.4M
Translational Research in Polycystic Ovary SyndromeU54HD034449 · NICHD · VIRGINIA COMMONWEALTH UNIVERSITY · PI ESSAH, PAULINA A · 1997 to 2012
$15.0M
INSULIN ACTION IN THE POLYCYSTIC OVARY SYNDROMER01DK040605 · NIDDK · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI DUNAIF, ANDREA · 1989 to 1997
–
NCRR NIH HHS M01 RR002635NCRR NIH HHS RR02635NICHD NIH HHS U54 HD034449NICHD NIH HHS U54 HD34449NIDDK NIH HHS R01 DK040605NIDDK NIH HHS R01 DK40605
6 · The paper itself

Abstract

Selective resistance to the effects of insulin on glucose metabolism in skeletal muscle and adipose tissue is a key feature of polycystic ovary syndrome (PCOS). The pathogenesis of insulin resistance in skeletal muscle in PCOS involves interaction of in vivo environmental factors with intrinsic defects in insulin signaling. We aimed to determine whether (1) intrinsic defects in insulin action/signaling and cytokine secretion were present in adipose cells in PCOS and (2) insulin resistance can be induced in control adipose cells by culture in medium conditioned by insulin-resistant PCOS fibroblasts. Subcutaneous abdominal preadipocytes from obese women with PCOS (n = 7) and age- and body mass index-matched controls (n = 5) were cultured for several generations in vitro. Basal and insulin-stimulated glycogen synthesis and basal glucose transport did not differ in the preadipocytes from women with PCOS and controls. Abundance of insulin receptor (IR) beta subunit, insulin receptor substrate (IRS) 1 and 2, p85 subunit of phosphatidylinositol 3-kinase, and extracellular signal-regulated kinase (ERK)1/2 activation did not differ. Secretion of tumor necrosis factor alpha and interleukin 6 did not differ. Insulin action on glycogen synthesis in control preadipocytes was not altered by coculture with or growth in media conditioned by PCOS skin fibroblasts with constitutive serine phosphorylation of IRbeta subunit (IR ser+), indicating that IR ser+ cells do not secrete an insulin resistance-inducing factor. We conclude that in contrast to skeletal muscle and skin fibroblasts, there is no evidence for intrinsic defects in insulin signaling in the PCOS adipose cell lineage, indicating that insulin resistance in these cells is likely due to factors in the in vivo environment.

Indexed as

AdipocytesAdultCell LineageExtracellular Signal-Regulated MAP KinasesFemaleGlucose Transport Proteins, FacilitativeGlycogenHumansInsulin Receptor Substrate ProteinsInsulin ResistanceInterleukin-6Intracellular Signaling Peptides and ProteinsPhosphatidylinositol 3-KinasesPhosphoproteinsPolycystic Ovary SyndromeReceptor, InsulinExtracellular Signal-Regulated MAP KinasesGlucose Transport Proteins, FacilitativeGlycogenInsulin Receptor Substrate ProteinsInterleukin-6Intracellular Signaling Peptides and ProteinsIRS1 protein, humanIRS2 protein, humanPhosphatidylinositol 3-KinasesPhosphoproteinsReceptor, InsulinTumor Necrosis Factor-alpha

Identifiers

PMID17445549
PMCPMC2427369
OpenAlexW2089631127

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.