4.3 Article

The effect of atorvastatin on pancreatic beta cell requirement in women with polycystic ovary syndrome

Journal

ENDOCRINE CONNECTIONS
Volume 6, Issue 8, Pages 811-816

Publisher

BIOSCIENTIFICA LTD
DOI: 10.1530/EC-17-0217

Keywords

polycystic ovary syndrome; statin; type 2 diabetes; insulin resistance

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Background: There is an increased risk of developing T2DM in women with polycystic ovary syndrome (PCOS), and there is evidence that statins improve metabolic parameters in these patients. However, there are some data to show that statins increase the risk of incipient diabetes. Materials and methods: We have previously shown that 12 weeks of atorvastatin improves insulin resistance when measured using HOMA-IR. This post hoc analysis was designed to look at the effect of atorvastatin on pancreatic beta cell function using HOMA-beta in the same study. In this randomised, double-blind placebo controlled study, 40 medication-naive patients with PCOS were randomised to either atorvastatin 20 mg daily or placebo for 3 months. A 3-month extension study for both groups of patients was undertaken with metformin 1500 mg daily after completing initial 3 months of atorvastatin or placebo. Results: There was a significant reduction in HOMA-beta (240 +/- 3.2 vs 177 +/- 2.3; P value < 0.01) after 12 weeks of atorvastatin treatment, which was maintained by metformin in the subsequent 12 weeks. There were no changes in HOMA-beta after the placebo or after subsequent metformin treatment. There was no linear correlation between reduction in HOMA-beta with improvement of free androgen index (FAI) (r(2) = 0.02; P = 0.72), testosterone (r(2) = 0.13; P = 0.49), SHBG (r2 = 0.22; P = 0.48), hsCRP (r(2) = 0.19; P = 0.64), triglycerides (r(2) = 0.09; P = 0.12), total cholesterol (r(2) = 0.11; P = 0.32) or LDL-C (r(2) = 0.19; P = 0.38). Conclusion: Treatment with atorvastatin for 12 weeks in women with PCOS significantly reduced HOMA-beta. This could be potentially due to fall in beta-cell requirement with improvement of insulin resistance rather than a reduction of beta-cell function.

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