Titre du document / Document title

Metabolic changes in human CD36 deficiency displayed by glucose loading

Auteur(s) / Author(s)

YANAI Hidekatsu ^{(1 2)} ; CHIBA Hitoshi ⁽¹⁾ ; FUJIWARA Hironobu ^{(1 2)} ; MORIMOTO Mie ⁽³⁾ ; TAKAHASHI Yukihiro ^{(1 2)} ; HUI Shu-Ping ⁽⁴⁾ ; FUDA Hirotoshi ⁽¹⁾ ; AKITA Harukuni ⁽¹⁾ ; KUROSAWA Takao ⁽⁴⁾ ; KOBAYASHI Kunihiko ⁽²⁾ ; MATSUNO Kazuhiko ⁽³⁾ ;

Affiliation(s) du ou des auteurs / Author(s) Affiliation(s)

⁽¹⁾ Department of Laboratory Medicine, Hokkaido University School of Medicine, Sapporo, JAPON
⁽²⁾ Department of Pediatrics, Hokkaido University School of Medicine, Sapporo, JAPON
⁽³⁾ College of Medical Technology, Hokkaido University, Sapporo, JAPON
⁽⁴⁾ Faculty of Pharmaceutical Sciences, the Health Sciences University of Hokkaido, Ishikari-Tobetsu, JAPON

Résumé / Abstract

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.

Revue / Journal Title

Thrombosis and haemostasis   ISSN 0340-6245   CODEN THHADQ 

Source / Source

2001, vol. 86, n^o4, pp. 995-999 (24 ref.)

Langue / Language

Anglais

Editeur / Publisher

Schattauer, Stuttgart, ALLEMAGNE  (1976) (Revue)

Mots-clés anglais / English Keywords

Genetic disease ; Metabolic diseases ; Human ; Pathophysiology ; Glucose ; Translocation ; Deficiency ; Carrier protein ; Triglyceride ; Fatty acids ; Biological transport ; Metabolism ; Lipids ;

Mots-clés français / French Keywords

Maladie héréditaire ; Métabolisme pathologie ; Antigène CD36 ; Homme ; Physiopathologie ; Glucose ; Translocation ; Déficit ; Protéine transport ; Triglycéride ; Acide gras ; Transport biologique ; Métabolisme ; Lipide ;

Mots-clés espagnols / Spanish Keywords

Enfermedad hereditaria ; Metabolismo patología ; Hombre ; Fisiopatología ; Glucosa ; Translocación ; Déficiencia ; Proteína transportador ; Triglicérido ; Acido graso ; Transporte biológico ; Metabolismo ; Lípido ;

Localisation / Location

INIST-CNRS, Cote INIST : 10255, 35400009646275.0110