Insulin secretion and sensitivity in non-obese and obese Japanese patients with coronary artery disease

Metabolism. 2002 Feb;51(2):184-8. doi: 10.1053/meta.2002.29985.


In a cross-sectional study of 240 patients with angiographically documented coronary artery disease (CAD), we investigated whether obese and non-obese subjects differed as to the influence of insulin deficiency and insulin resistance on glucose intolerance and cardiovascular risk. Patients were classified according to a 75-g oral glucose tolerance test as having normal glucose tolerance (NGT), impaired glucose tolerance (IGT), or diabetes mellitus (DM). We defined obesity as a body mass index (BMI) exceeding 25 kg/m(2). Early phase insulin secretion (insulinogenic index) declined with worsening glucose intolerance in non-obese (tau = -.216, P <.001; Kendall's correlation coefficient) and obese subjects (tau = -.392, P <.001). Total insulin secretion was higher in obese subjects with NGT or IGT than in controls and decreased in association with worsening glucose intolerance in obese subjects (tau = -.239, P <.001). Insulin sensitivity was calculated by 3 proposed indices. The first of these decreased in association with worsening in glucose tolerance in non-obese subjects (tau = -.137, P <.01). The second showed such a pattern in both groups (non-obese, tau = -.407, P <.001; obese, tau = -.311, P <.001), as did the third (non-obese, tau = -.512, P <.001; obese, tau = -.488, P < 0.001). Because even prediabetic Japanese subjects with CAD showed a latent insulin secretion defect in response to a glucose load, as well as impaired insulin sensitivity, compensatory hyperinsulinemia is not a sensitive indicator of coronary risk.

Publication types

  • Comparative Study

MeSH terms

  • Aged
  • Coronary Artery Disease / complications*
  • Coronary Artery Disease / metabolism
  • Coronary Artery Disease / physiopathology
  • Humans
  • Insulin / metabolism*
  • Insulin Resistance*
  • Insulin Secretion
  • Japan
  • Middle Aged
  • Obesity / complications*
  • Obesity / metabolism
  • Obesity / physiopathology


  • Insulin