Thromb Haemost 2001; 86(04): 995-999
DOI: 10.1055/s-0037-1616523
Special Article
Schattauer GmbH

Metabolic Changes in Human CD36 Deficiency Displayed by Glucose Loading

Authors

  • Hidekatsu Yanai

    1   Departments of Laboratory Medicine, Sapporo
    2   Pediatrics, Hokkaido University School of Medicine, Sapporo
  • Hitoshi Chiba

    1   Departments of Laboratory Medicine, Sapporo
  • Hironobu Fujiwara

    1   Departments of Laboratory Medicine, Sapporo
    2   Pediatrics, Hokkaido University School of Medicine, Sapporo
  • Mie Morimoto

    3   College of Medical Technology, Hokkaido University, Sapporo
  • Yukihiro Takahashi

    1   Departments of Laboratory Medicine, Sapporo
    2   Pediatrics, Hokkaido University School of Medicine, Sapporo
  • Shu-Ping Hui

    4   Faculty of Pharmaceutical Sciences, the Health Sciences University of Hokkaido, Ishikari-Tobetsu, Japan
  • Hirotoshi Fuda

    1   Departments of Laboratory Medicine, Sapporo
  • Harukuni Akita

    1   Departments of Laboratory Medicine, Sapporo
  • Takao Kurosawa

    4   Faculty of Pharmaceutical Sciences, the Health Sciences University of Hokkaido, Ishikari-Tobetsu, Japan
  • Kunihiko Kobayashi

    2   Pediatrics, Hokkaido University School of Medicine, Sapporo
  • Kazuhiko Matsuno

    3   College of Medical Technology, Hokkaido University, Sapporo
Further Information

Publication History

Received 02 February 2001

Accepted after resubmission 14 May 2001

Publication Date:
09 December 2017 (online)

Preview

Summary

Previous in vitro studies have shown that CD36 participates in cellular fatty acid (FA) uptake. In vivo evidence for a physiologic role of CD36 in this process is poor and mostly obtained in animals. To examine the metabolic role of human CD36, we performed a glucose loading test for normals (n = 16) and subjects with CD36 deficiency, both Type I (n = 5) and Type II (n = 16). After 30 min, FA levels had fallen by 60.1% in normals but by only 31.7% in Type II deficiency (P <0.01 vs. normals) and 16.5% in Type I deficiency which remained significantly higher than the other two groups out to 2 h. Further, changes in triglyceride and glucose metabolism were observed in the both types of CD36 deficiency. Impaired fast FA clearance by muscle and consequently increased hepatic FA uptake seem to underlie these changes. We conclude that human CD36 deficiency causes systemic metabolic changes.