Metabolic Changes in Human CD36 Deficiency Displayed by Glucose Loading
Metabolic Changes in Human CD36 Deficiency Displayed by Glucose Loading
复制标题
葡萄糖负荷显示人类 CD36 缺乏症的代谢变化
DOI：
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发表时间：
2001
影响因子：
6.7
通讯作者：
K. Matsuno
中科院分区：
文献类型：
--
作者：
H. Yanai;H. Chiba;H. Fujiwara;M. Morimoto;Yukihiro Takahashi;S. Hui;H. Fuda;H. Akita;T. Kurosawa;K. Kobayashi;K. Matsuno
摘要先前的体外研究表明CD36参与了细胞脂肪酸(FA)的摄取。CD36在这一过程中发挥生理作用的体内证据很少，主要是在动物身上获得的。为了研究人类CD36的代谢作用，我们对正常人(n=16)和CD36缺乏症患者进行了葡萄糖负荷试验，包括I型(n=5)和II型(n=16)。30min后，正常组的FA水平下降了60.1%，而II型缺陷组下降了31.7%(P<；0.01 vs正常)，I型缺陷组下降了16.5%，直至2小时仍显著高于其他两组。肌肉对FA的快速清除受损，从而增加了肝脏对FA的摄取，似乎是这些变化的基础。我们的结论是，人类CD36缺乏会引起全身代谢变化。
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.
胰岛素通过其磷脂酰肌醇锚的代谢刺激脂蛋白脂肪酶的释放。
DOI：
10.1126/science.241.4873.1670
发表时间：
1988
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Chan,BL;Lisanti,MP;Rodriguez-Boulan,E;Saltiel,AR
通讯作者：
Saltiel,AR
DOI：
10.1073/pnas.93.7.2646
发表时间：
1996-04-02
影响因子：
11.1
作者：
Ibrahimi, A;Sfeir, Z;Abumrad, NA
通讯作者：
Abumrad, NA