Insulin secretory defects in polycystic ovary syndrome. Relationship to insulin sensitivity and family history of non-insulin-dependent diabetes mellitus.

Ehrmann, D A; Sturis, J; Byrne, M M; Karrison, T; Rosenfield, R L; Polonsky, K S

doi:10.1172/jci118064

Cited by 426Ovarian function and disordersPancreatic function and diabetesDiabetes, Cardiovascular Risks, and Lipoproteins

Insulin secretory defects in polycystic ovary syndrome. Relationship to insulin sensitivity and family history of non-insulin-dependent diabetes mellitus.

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Ehrmann, D A, Sturis, J, Byrne, M M, Karrison, T, Rosenfield, R L, Polonsky, K S·1995·Journal of Clinical Investigation

DOI 10.1172/jci118064PMC PMC185226

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Abstract

The increased prevalence of non-insulin-dependent diabetes mellitus (NIDDM) among women with polycystic ovary syndrome (PCOS) has been ascribed to the insulin resistance characteristic of PCOS. This study was undertaken to determine the role of defects in insulin secretion as well as familial factors to the predisposition to NIDDM seen in PCOS. We studied three groups of women: PCOS with a family history of NIDDM (PCOS FHx POS; n = 11), PCOS without a family history of NIDDM (PCOS FHx NEG; n = 13), and women without PCOS who have a family history of NIDDM (NON-PCOS FHx POS; n = 8). Beta cell function was evaluated during a frequently sampled intravenous glucose tolerance test, by a low dose graded glucose infusion, and by the ability of the beta cell to be entrained by an oscillatory glucose infusion. PCOS FHx POS women were significantly less likely to demonstrate appropriate beta cell compensation for the degree of insulin resistance. The ability of the beta cell to entrain, as judged by the spectral power for insulin secretion rate, was significantly reduced in PCOS FHx POS subjects. In conclusion, a history of NIDDM in a first-degree relative appears to define a subset of PCOS subjects with a greater prevalence of insulin secretory defects. The risk of developing NIDDM imparted by insulin resistance in PCOS may be enhanced by these defects in insulin secretion.

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Subjects at high risk of developing Type 2 diabetes, including first-degree relatives, women with a history of gestational diabetes or polycystic ovarian disease, older subjects, and subjects with impaired glucose tolerance, have diminished beta-cell function, manifest as a reduced first-phase insulin response to intravenous glucose relative to insulin sensitivity, even when many still have NGT.
“Based on the concept of a feedback loop, it has become evident that subjects who are at high risk of developing Type 2 diabetes have diminished beta-cell function at a time when many of them still have NGT.”
From The relative contributions of insulin resistance and beta-cell dysfunction to the pathophysiology of type 2 diabetes (2003) · cites this paper as [96]

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Regulation of HOXA-10 Expression by Testosterone in Vitro and in the Endometrium of Patients with Polycystic Ovary Syndrome
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Glucose Intolerance in a Large Cohort of Mediterranean Women With Polycystic Ovary Syndrome
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Prevalence and determinants of gestational diabetes mellitus in Africa based on the updated international diagnostic criteria: A systematic review and meta-analysis
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Evaluation of Adverse Outcome in Young Women with Polycystic Ovary SyndromeVersusMatched, Reference Controls: A Retrospective, Observational Study
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Polycystic Ovary Syndrome and Obstructive Sleep Apnea
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Beta-Cell Function in Polycystic Ovary Syndrome
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Beta cell function and insulin sensitivity in women with polycystic ovary syndrome: Influence of the family history of type 2 diabetes mellitus
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Insulin secretion in women with polycystic ovary syndrome
Grimmichová, T. (2009) · Digital Repository (National Repository of Grey Literature)
Beta-cell dysfunction independent of obesity and glucose intolerance in the polycystic ovary syndrome
Dunaif, A. E., & Finegood, D. T. (1996) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jcem.81.3.8772555 · Cited by 454 · see citing works

Authors: Ehrmann, D. A., Sturis, J., Byrne, M. M., Karrison, T., Rosenfield, R. L., & Polonsky, K. S.
Affiliations: University of Chicago (US)
ORCID: Sturis, J
Byrne, M M
Karrison, T
Rosenfield, R L
Venue: Journal of Clinical Investigation
Publisher: American Society for Clinical Investigation
Published: 1995-07-01
Volume: 96
Issue: 1
Pages: 520-527
ISSN: 0021-9738 (ISSN-L)
DOI: 10.1172/jci118064
PMC: PMC185226
OpenAlex: W2100224373
Cited by: 426
References: 52
Citations by year: 2025: 1 · 2024: 6 · 2023: 5 · 2022: 12 · 2021: 5 · 2020: 5 · 2019: 9 · 2018: 6 · 2017: 13 · 2016: 11 · 2015: 17 · 2014: 10 · 2013: 12 · 2012: 23
FWCI: 13.28
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Journal of Clinical Investigation (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: National Institute of Diabetes and Digestive and Kidney Diseases (DK 07011-7, T32DK007011)
National Center for Research Resources (RR-00055)
Eunice Kennedy Shriver National Institute of Child Health and Human Development (HD 06308, R01HD006308)
Topics: Health Sciences › Medicine › Reproductive Medicine › Ovarian function and disorders
Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
Keywords: polycystic ovary syndrome, insulin secretion, insulin resistance, type 2 diabetes, family history of diabetes, beta-cell function, beta-cell compensation, glucose infusion, insulin secretion rate, insulin sensitivity
MeSH terms: Insulin Secretion, Adult, Blood Glucose, Diabetes Mellitus, Type 2, Female, Glucose, Glucose Tolerance Test, Humans, Insulin, Insulin Resistance, Polycystic Ovary Syndrome, Testosterone, Body Mass Index

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Insulin secretory defects in polycystic ovary syndrome. Relationship to insulin sensitivity and family history of non-insulin-dependent diabetes mellitus.

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