Feedback inhibition of insulin secretion and insulin resistance in polycystic ovarian syndrome with and without obesity

Eur Rev Med Pharmacol Sci. Sep-Oct 1997;1(5):167-71.

Abstract

Hyperinsulinemia/insulin resistance is a well-known feature of polycystic ovarian (PCO) syndrome. In this study, the comparative roles of the peripheral tissues and the pancreatic beta-cells in its pathogenesis were evaluated. We determined basal serum C-peptide values (index of insulin secretion) and in vivo insulin action on peripheral glucose utilization (by the euglycemic hyperinsulinemic clamp technique) in obese (n = 5) and nonobese (n = 5) PCO women compared to obese (n = 5) and nonobese (n = 5) normal ovulatory women. During the clamp, feed-back inhibition of insulin on insulin secretion was studied by C-peptide percentage suppression. Serum C-peptide basal values did not differ significantly between the four groups. Insulin stimulated glucose utilization, expressed as M-value, was significantly decreased in both PCO groups compared to normal ovulatory women (p < 0.005). The metabolic clearance rate of glucose (MCR) and insulin (M/I) had the same behaviour. No differences were found between M, MCR and M/I values and the two groups of PCO subjects (obese/nonobese). The C-peptide percentage suppression was similar in all the groups. We conclude that PCO women have a significant insulin resistance that is independent of obesity, while basal and insulin-inhibited insulin secretion do not differ from normal-cycle subjects.

Publication types

  • Clinical Trial

MeSH terms

  • Adult
  • Feedback / physiology
  • Female
  • Humans
  • Insulin / metabolism*
  • Insulin Resistance / physiology*
  • Insulin Secretion
  • Obesity / complications
  • Obesity / metabolism*
  • Polycystic Ovary Syndrome / complications
  • Polycystic Ovary Syndrome / metabolism*

Substances

  • Insulin