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This Article Full Text Full Text (PDF) All Versions of this Article: 287/2/E241    most recent 00475.2003v2 00475.2003v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (8) Citing Articles via Google Scholar Google Scholar Articles by Ehrmann, D. A. Articles by Polonsky, K. S. Search for Related Content PubMed PubMed Citation Articles by Ehrmann, D. A. Articles by Polonsky, K. S.

Impaired -cell compensation to dexamethasone-induced hyperglycemia in women with polycystic ovary syndrome

¹Department of Medicine, University of Chicago, Chicago, Illinois 60637; ²Department of Electronics and Informatics, University of Padua, Padua, 35131 Italy; and ³Department of Medicine, Washington University School of Medicine, St. Louis, Missouri 63110

Submitted 22 October 2003 ; accepted in final form 1 December 2003

Deterioration in glucose tolerance occurs rapidly in women with polycystic ovary syndrone (PCOS), suggesting that pancreatic -cell dysfunction may supervene early. To determine whether the compensatory insulin secretory response to an increase in insulin resistance induced by the glucocorticoid dexamethasone differs in women with PCOS and control subjects, we studied 10 PCOS and 6 control subjects with normal glucose tolerance. An oral glucose tolerance test (OGTT) and a graded glucose infusion protocol were performed at baseline and after subjects took 2.0 mg of dexamethasone orally. Basal (_b), static (_s), dynamic (_d), and global () indexes of -cell sensitivity to glucose were derived. Insulin sensitivity (S_i) was calculated using the minimal model; a disposition index (DI) was calculated as the product of S_i and . PCOS and control subjects had nearly identical fasting and 2-h glucose levels at baseline. _b was higher, although not significantly so, in the PCOS subjects. The _d, _s, and indexes were 28, 19, and 20% higher, respectively, in PCOS subjects. The DI was significantly lower in PCOS (30.01 ± 5.33 vs. 59.24 ± 7.59) at baseline. After dexamethasone, control subjects averaged a 9% increase (to 131 ± 12 mg/dl) in 2-h glucose levels; women with PCOS had a significantly greater 26% increase to 155 ± 6 mg/dl. The C-peptide-to-glucose ratios on OGTT increased by 44% in control subjects and by only 15% in PCOS subjects. The accelerated deterioration in glucose tolerance in PCOS may result, in part, from a relative attenuation in the response of the -cell to the demand placed on it by factors exacerbating insulin resistance.

insulin resistance; insulin secretion; type 2 diabetes

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