Metformin has no major effects on glucose homeostasis in pregnant women with PCOS: results of a randomized double‐blind study

Abstract

Objective. Previous non‐randomized and uncontrolled studies indicate major metformin effects on glucose homeostasis in pregnant women with polycystic ovary syndrome (PCOS). We investigated metformin effects on glucose homeostasis in a prospective controlled study. Material and methods. Forty pregnant women with PCOS and without known diabetes mellitus were included in the first trimester and randomized to either metformin 850 mg twice daily or placebo. Outcome measures were fasting glucose and insulin at inclusion and changes to pregnancy weeks 19, 32 and 36 and 2 h glucose levels during a 75 g oral glucose tolerance test (OGTT) carried out at inclusion and pregnancy weeks 19 and 32. Insulin resistance (HOMA‐IR) and beta‐cell function (HOMA‐β) were calculated using the homeostasis assessment model. Results. At inclusion, 2 h glucose levels during OGTT were higher in the placebo group (7.14 versus 6.03 mmol/L; p = 0.012). Accordingly, 6 out of 22 in the metformin group versus 2 out of 18 women in the placebo group (p = 0.21) had gestational diabetes mellitus at inclusion. At gestational weeks 19 and 32, 2‐h plasma glucose levels were equal between the groups. The total proportion of women with gestational diabetes did not differ between the groups, nor did any of the other indices of glucose metabolism and insulin resistance. Conclusions. Metformin seems to be without major effects on glucose homeostasis in pregnant women with PCOS.

• Gestational diabetes
• glucose
• insulin resistance
• polycystic ovary syndrome
• pregnancy

Acknowledgements

We thank Harriet Selle, a specialist nurse in diabetes, for her help in management and care of the patients. The study was supported by the Norwegian Women's Public Health Association. Metformin was supplied free of charge by Weifa A/S, Oslo, Norway.

Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.