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Increased Risk Factors for Coronary Artery Disease in Japanese Subjects With Hyperinsulinemia or Glucose Intolerance

  1. Nobuhiro Yamada, MD,
  2. Hideyo Yoshinaga, MD,
  3. Noboru Sakurai, MD,
  4. Hitoshi Shimano, MD,
  5. Takanari Gotoda, MD,
  6. Yasuo Ohashi, PHD,
  7. Yoshio Yazaki, MD and
  8. Kinori Kosaka, MD
  1. Department of Internal Medicine Tokyo, Japan
  2. Department of Epidemiology Tokyo, Japan
  3. University of Tokyo, Toranomon Hospital Tokyo, Japan
  1. Address correspondence and reprint requests to Nobuhiro Yamada, MD, 3rd Department of Internal Medicine, University of Tokyo, Tokyo, Japan 113.

Abstract

OBJECTIVE To understand the interrelationship of coronary artery disease (CAD) risk factors including hyperlipidemia, hypertension, and glucose intolerance to prevent and better manage this disease.

RESEARCH DESIGN AND METHODS We performed a 100-g oral glucose tolerance test in 2,113 subjects, and we evaluated their plasma lipid levels, blood pressure (BP), and plasma glucose and plasma insulin responses.

RESULTS Multiple regression analysis demonstrated a significant relationship of either BP, plasma triglyceride (TG), or high-density lipoprotein (HDL) cholesterol levels to plasma insulin and glucose response after the glucose load. Plasma cholesterol levels were related only to the plasma glucose response. In subjects matched for age, sex, and body mass index (BMI) with hyperinsulinemia or normoinsulinemia, the hyperinsulinemic subjects had a significantly higher mean BP and plasma TG level than the normoinsulinemic subjects (128.8/82.3 vs. 122.9/79.3 mmHg and 172.1 vs. 119.4 mg/dl), and the HDL-cholesterol level was significantly lower (43.9 vs. 47.8 mg/dl). Furthermore, subjects matched for age, sex, and BMI with glucose intolerance had a higher mean BP (128.4/81.8 vs. 123.5/78.7 mmHg) and higher plasma TG level (154.2 vs. 123.0 mg/dl) than those without glucose intolerance.

CONCLUSIONS Based on these findings, subjects with hyperinsulinemia or glucose intolerance should be carefully managed to prevent CAD, because they have more numerous and more severe risk factors than subjects with normal plasma insulin levels or subjects without glucose intolerance.

  • Received November 30, 1992.
  • Accepted August 19, 1993.
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