Original ArticlePancreatic β-CELL Dysfunction in Polycystic Ovary Syndrome: the Role of Metformin
Section snippets
INTRODUCTION
Polycystic ovary syndrome (PCOS) occurs in approximately 6% to 7% of women of reproductive age (1) and is arguably the most common endocrine disorder in women (2, 3, 4). The syndrome is defined by 2 of the following 3 features: (a) oligo-ovulation or anovulation, (b) clinical and/ or biochemical signs of hyperandrogenism, and (c) polycystic ovaries (5). This definition assumes the exclusion of other disorders that might present in a similar fashion (5). Studies show that up to 90% of women with
METHODS
We prospectively enrolled women with PCOS from a private practice and from the Mount Sinai Hospital Endocrinology Clinic from January 2009 until June 2010. We documented age, self-reported race/ethnicity, body mass index, and testosterone concentration. Family history of type 2 diabetes mellitus was noted. All study participants met 2 of the 3 revised 2003 Rotterdam European Society for Human Reproduction/American Society of Reproductive Medicine PCOS Consensus Workshop Group diagnostic
DISCUSSION
Many studies have examined β-cell function in PCOS, and thus far, the results are equivocal. Several studies have shown that there is a defect in glucose-stimulated insulin secretion (11,19,20). However, other studies have shown that patients with PCOS have an increased insulin response, probably as compensation for peripheral insulin resistance (21, 22, 23, 24).Finally, some investigators have demonstrated entirely normal first-phase insulin secretion in patients with PCOS (25,26). This
CONCLUSION
We determined that metformin does not lead to a significant change in AIRg, insulin sensitivity, or disposition index in patients with PCOS. However, the proportionate change in disposition index after metformin treatment correlated significantly with the proportionate change in insulin sensitivity. These data suggest that AIRg did not respond appropriately to changes in insulin sensitivity and may indicate a β-cell defect in patients with PCOS. Further research is needed to define the
DISCLOSURE
The authors have no multiplicity of interest to disclose.
ACKNOWLEDGMENT
This study was funded by the Endocrine Fellows’ Foundation and New York Community Trust RME.
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