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

Cellular mechanisms of insulin resistance in polycystic ovarian syndrome

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

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.

Integrity signals

Registry

Crossref · 10.1210/jc.75.2.577

Cites

21 of 21 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

We couldn’t retrieve this paper’s full text, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Ciaraldi, T. P.
Affiliations
University of California System (US)
Venue
Journal of Clinical Endocrinology & Metabolism
Published
1992-08-01
Volume
75
Issue
2
Pages
577-583
ISSN
0021-972X (ISSN-L)
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

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review