Cited by 336Ovarian function and disordersMetabolism, Diabetes, and CancerDiabetes, Cardiovascular Risks, and Lipoproteins

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Cellular mechanisms of insulin resistance in polycystic ovarian syndrome

Ciaraldi, T. P.·1992·Journal of Clinical Endocrinology & Metabolism

DOI 10.1210/jc.75.2.577

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Abstract

Insulin resistance is a predominant feature in women with polycystic ovarian syndrome (PCO). The cellular mechanisms for this insulin resistance have not been defined. In this study, major steps in the insulin action cascade, receptor binding, kinase activity, and glucose transport activity were evaluated in isolated adipocytes prepared from PCO subjects (n = 8) without acanthosis nigricans and in a group of age and weight-matched controls [normal cycling (NC) n = 8]. The PCO group was hyperinsulinemic and displayed elevated insulin responses to an iv glucose load. The binding of 125I-insulin to adipocytes was similar in cells from PCO and NC subjects. In PCO, autophosphorylation of the insulin receptor-subunit in the absence of insulin was normal but a significant decrease (30% below control) in maximal insulin stimulated autophosphorylation was observed. However, receptor kinase activity measured against the exogenous substrate poly glu:tyr (4:1) was normal. Cells from PCO subjects transported glucose at the same rate, in both the absence and presence of a maximal insulin concentration, as those from NC subjects. Strikingly, there was a large rightward shift in the insulin dose-response curve for transport stimulation in PCO cells (EC50 = 87 +/- 14 pmol in NC vs. 757 +/- 138 in PCO, P less than 0.0005); 8-fold greater insulin concentrations were required to attain comparable glucose transport rates in cells from PCO against NC. In conclusion, our results suggest that insulin resistance in PCO, as assessed in the adipocyte, is accompanied by normal function of insulin receptors, but involves a novel postreceptor defect in the insulin signal transduction chain between the receptor kinase and glucose transport.

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Authors: Ciaraldi, T. P.
Affiliations: University of California System (US)
ORCID: Ciaraldi, T. P.
Venue: Journal of Clinical Endocrinology & Metabolism
Publisher: The Endocrine Society
Published: 1992-08-01
Volume: 75
Issue: 2
Pages: 577-583
ISSN: 0021-972X (ISSN-L)
DOI: 10.1210/jc.75.2.577
OpenAlex: W2028242557
Cited by: 336
References: 21
Citations by year: 2026: 1 · 2025: 6 · 2024: 3 · 2023: 6 · 2022: 13 · 2021: 11 · 2020: 11 · 2019: 7 · 2018: 8 · 2017: 8 · 2016: 7 · 2015: 7 · 2014: 4 · 2013: 13 · 2012: 8
FWCI: 6.58
Type: journal article
Language: en
Open access: closed
Locations: The Journal of Clinical Endocrinology & Metabolism (publishedVersion)
PubMed (publishedVersion)
Funders: National Institute of Diabetes and Digestive and Kidney Diseases (DK-33649, DK-33651)
NIH Clinical Center
Eunice Kennedy Shriver National Institute of Child Health and Human Development (HD-12303-14)
Topics: Health Sciences › Medicine › Reproductive Medicine › Ovarian function and disorders
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
Keywords: insulin resistance, polycystic ovary syndrome, adipocytes, insulin receptor autophosphorylation, glucose transport, insulin signaling, postreceptor defect, hyperinsulinemia, insulin dose-response
MeSH terms: Adipose Tissue, Adolescent, Adult, Female, Glucose Tolerance Test, Humans, Injections, Intravenous, Insulin, Insulin Resistance, Monosaccharide Transport Proteins, Polycystic Ovary Syndrome, Protein-Tyrosine Kinases, Receptor, Insulin, Reference Values

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Cellular mechanisms of insulin resistance in polycystic ovarian syndrome

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