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Metabolic and Steroidogenic Alterations Related to Increased Frequency of Polycystic Ovaries in Women with a History of Gestational Diabetes¹

Departments of Obstetrics and Gynecology (R.M.K., J.J., L.C.M.-P., J.S.T.) and Clinical Chemistry (A.R.), University Hospital of Oulu, 90220 Oulu; and Department of Medicine, University Hospital of Kuopio (I.V.), 70210 Kuopio, Finland

Address all correspondence and requests for reprints to: Dr. J. S. Tapanainen, Department of Obstetrics and Gynecology, University Hospital of Oulu, Kajaanintie 52 A, FIN-90220 Oulu, Finland. E-mail: juha.tapanainen{at}oulu.fi

Abstract

The prevalence of polycystic ovaries (PCO) and clinical, endocrine, and metabolic features were investigated in women with previous gestational diabetes (GDM). Thirty-three women with a history of GDM and 48 controls were studied. Glucose and insulin secretion capacity was evaluated by means of the oral glucose tolerance test (OGTT), and insulin action was determined by means of a euglycemic insulin clamp. Compared with control women, women with previous GDM more often had significantly abnormal OGTT, a higher prevalence of PCO (39.4% vs. 16.7%; P = 0.03), higher serum concentrations of cortisol, dehydroepiandrosterone, and dehydroepiandrosterone sulfate and a greater area under the glucose curve.

Women with previous GDM showed a lowered early phase insulin response to glucose and impaired insulin sensitivity, which was accounted for mainly by decreased glucose nonoxidation. They also demonstrated a significantly lower fasting serum C peptide/insulin ratio than the controls, indicating that women with previous GDM have impaired hepatic insulin extraction, which tended to be more marked among women with PCO. This may explain why women with PCO and previous GDM were significantly more hyperinsulinemic than women with normal ovaries.

In conclusion, our data demonstrate that women with previous GDM often have PCO and abnormal OGTT. They are insulin resistant as a result of lowered glucose nonoxidation and show inappropriately low insulin responses to glucose, reflecting impaired ß-cell function. They also have higher adrenal androgen secretion, which may be associated with abdominal obesity.

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