Yanai H, Chiba H, Fujiwara H, Morimoto M, Takahashi Y, Hui S P, Fuda H, Akita H, Kurosawa T, Kobayashi K, Matsuno K
Department of Laboratory Medicine, Hokkaido University School of Medicine, Sapporo, Japan.
Thromb Haemost. 2001 Oct;86(4):995-9.
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.
以往的体外研究表明，CD36参与细胞脂肪酸（FA）摄取。CD36在此过程中的生理作用的体内证据不足，且大多来自动物实验。为了研究人类CD36的代谢作用，我们对正常受试者（n = 16）以及I型（n = 5）和II型（n = 16）CD36缺乏症患者进行了葡萄糖负荷试验。30分钟后，正常受试者的FA水平下降了60.1%，而II型缺乏症患者仅下降了31.7%（与正常受试者相比，P <0.01），I型缺乏症患者下降了16.5%；在长达2小时的时间内，I型缺乏症患者的FA水平仍显著高于其他两组。此外，在两种类型的CD36缺乏症中均观察到甘油三酯和葡萄糖代谢的变化。肌肉对FA的快速清除受损，进而导致肝脏对FA的摄取增加，似乎是这些变化的潜在原因。我们得出结论，人类CD36缺乏会导致全身代谢变化。
