Metabolic and steroidogenic alterations related to increased frequency of polycystic ovaries in women with a history of gestational diabetes

Citation
Rm. Koivunen et al., Metabolic and steroidogenic alterations related to increased frequency of polycystic ovaries in women with a history of gestational diabetes, J CLIN END, 86(6), 2001, pp. 2591-2599
Citations number
62
Categorie Soggetti
Endocrynology, Metabolism & Nutrition","Endocrinology, Nutrition & Metabolism
Journal title
JOURNAL OF CLINICAL ENDOCRINOLOGY AND METABOLISM
ISSN journal
0021972X → ACNP
Volume
86
Issue
6
Year of publication
2001
Pages
2591 - 2599
Database
ISI
SICI code
0021-972X(200106)86:6<2591:MASART>2.0.ZU;2-C
Abstract
The prevalence of polycystic ovaries (PCO) and clinical, endocrine, and met abolic features were investigated in women with previous gestational diabet es (GDM). Thirty-three women with a history of GDM and 48 controls were stu died. Glucose and insulin secretion capacity was evaluated by means of the oral glucose tolerance test (OGTT), and insulin action was determined by me ans of a euglycemic insulin clamp. Compared with control women, women with previous GDM more often had significantly abnormal OGTT, a higher prevalenc e of PCO (39.4% vs. 16.7%; P = 0.03), higher serum concentrations of cortis ol, dehydroepiandrosterone, and dehydroepiandrosterone sulfate and a greate r area under the glucose curve. Women with previous GDM showed a lowered early phase insulin response to gl ucose and impaired insulin sensitivity, which was accounted for mainly by d ecreased glucose nonoxidation. They also demonstrated a significantly lower fasting serum C peptide/insulin ratio than the controls, indicating that w omen with previous GDM have impaired hepatic insulin extraction, which tend ed to be more marked among women with PCO. This may explain why women with PCO and previous GDM were significantly more hyperinsulinemic than women wi th 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 g lucose nonoxidation and show inappropriately low insulin responses to gluco se, reflecting impaired beta -cell function. They also have higher adrenal androgen secretion, which may be associated with abdominal obesity.