Evidence map›Paper›PMID 25714674›Full record

ArticleAmerican journal of physiology. Endocrinology and metabolism2015

Pancreatic β-cell dysfunction in polycystic ovary syndrome: role of hyperglycemia-induced nuclear factor-κB activation and systemic inflammation.

Steven K Malin, John P Kirwan, Chang Ling Sia, Frank González

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Endocrinology and metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
5.1field-weighted citation impact, top 6% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

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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.

Steven K MalinDepartment of Pathobiology, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio; Department of Nutrition, School of Medicine, Case Western Reserve University, Cleveland, Ohio; and.
John P KirwanDepartment of Pathobiology, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio; Department of Nutrition, School of Medicine, Case Western Reserve University, Cleveland, Ohio; and.
Chang Ling SiaDepartment of Obstetrics and Gynecology, Indiana University School of Medicine, Indianapolis, Indiana.
Frank GonzálezDepartment of Obstetrics and Gynecology, Indiana University School of Medicine, Indianapolis, Indiana gonzalef@iupui.edu.
Case Western Reserve University · USIndiana University – Purdue University Indianapolis · USIndiana University School of Medicine

Funding

Clinical and Translational Science Collaborative of ClevelandUL1TR000439 · NCATS · CASE WESTERN RESERVE UNIVERSITY · PI KONSTAN, MICHAEL W. · 2012 to 2016
$50.0M
TRAINING IN METABOLISMT32DK007319 · NIDDK · CASE WESTERN RESERVE UNIVERSITY · PI BRUNENGRABER, HENRI · 1986 to 2013
$5.0M
Age, Exercise, Diet: Effects on Insulin ResistanceR01AG012834 · NIA · CLEVELAND CLINIC LERNER COM-CWRU · PI KIRWAN, JOHN P. · 2004 to 2008
$1.9M
Inflammation: Effect on Insulin Resistance in PCOSR03HD048535 · NICHD · MAYO CLINIC ROCHESTER · PI GONZALEZ, FRANK · 2006 to 2007
$146k
NCATS NIH HHS UL1 TR000439NIA NIH HHS R01-AG-12834NICHD NIH HHS HD-048535NIDDK NIH HHS T32-DK-007319
6 · The paper itself

Abstract

In polycystic ovary syndrome (PCOS), oxidative stress is implicated in the development of β-cell dysfunction. However, the role of mononuclear cell (MNC)-derived inflammation in this process is unclear. We determined the relationship between β-cell function and MNC-derived nuclear factor-κB (NF-κB) activation and tumor necrosis factor-α (TNF-α) secretion in response to a 2-h 75-g oral glucose tolerance test (OGTT) in normoglycemic women with PCOS (15 lean, 15 obese) and controls (16 lean, 14 obese). First- and second-phase β-cell function was calculated as glucose-stimulated insulin secretion (insulin/glucose area under the curve for 0-30 and 60-120 min, respectively) × insulin sensitivity (Matsuda Index derived from the OGTT). Glucose-stimulated NF-κB activation and TNF-α secretion from MNC, and fasting plasma thiobarbituric acid-reactive substances (TBARS) and high-sensitivity C-reactive protein (hs-CRP) were also assessed. In obese women with PCOS, first- and second-phase β-cell function was lower compared with lean and obese controls. Compared with lean controls, women with PCOS had greater change from baseline in NF-κB activation and TNF-α secretion, and higher plasma TBARS. β-Cell function was inversely related to NF-κB activation (1st and 2nd) and TNF-α secretion (1st), and plasma TBARS and hs-CRP (1st and 2nd). First- and second-phase β-cell function also remained independently linked to NF-κB activation after adjustment for body fat percentage and TBARS. In conclusion, β-cell dysfunction in PCOS is linked to hyperglycemia-induced NF-κB activation from MNC and systemic inflammation. These data suggest that in PCOS, inflammation may play a role in impairing insulin secretion before the development of overt hyperglycemia.

Indexed as

HyperglycemiaInflammationAdolescentAdultCase-Control StudiesCells, CulturedFemaleGlucose Tolerance TestHumansInsulin-Secreting CellsNF-kappa BObesityPolycystic Ovary SyndromeYoung AdultNF-kappa Bandrogensglucose intoleranceinsulin resistanceinsulin secretioninsulin sensitivitymononuclear cellsobesity

Identifiers

PMID25714674
PMCPMC4420895
OpenAlexW1991962739

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.