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本文引用的文献

1
Coimmunoprecipitation of FAT/CD36 and CPT I in skeletal muscle increases proportionally with fat oxidation after endurance exercise training.耐力运动训练后,骨骼肌中FAT/CD36与肉碱棕榈酰转移酶I的共免疫沉淀与脂肪氧化成比例增加。
Am J Physiol Endocrinol Metab. 2006 Aug;291(2):E254-60. doi: 10.1152/ajpendo.00051.2006. Epub 2006 May 2.
2
Identification of fatty acid translocase on human skeletal muscle mitochondrial membranes: essential role in fatty acid oxidation.人骨骼肌线粒体膜上脂肪酸转运蛋白的鉴定:在脂肪酸氧化中的重要作用。
Am J Physiol Endocrinol Metab. 2006 Mar;290(3):E509-15. doi: 10.1152/ajpendo.00312.2005. Epub 2005 Oct 11.
3
Regulation of fatty acid transport by fatty acid translocase/CD36.脂肪酸转位酶/CD36对脂肪酸转运的调控
Proc Nutr Soc. 2004 May;63(2):245-9. doi: 10.1079/PNS2004331.
4
Metabolic changes in human CD36 deficiency displayed by glucose loading.葡萄糖负荷显示的人类CD36缺乏症中的代谢变化。
Thromb Haemost. 2001 Oct;86(4):995-9.
5
Phenotype-genotype correlation in CD36 deficiency types I and II.I型和II型CD36缺乏症的表型-基因型相关性
Thromb Haemost. 2000 Sep;84(3):436-41.
6
Defective uptake and utilization of long chain fatty acids in muscle and adipose tissues of CD36 knockout mice.CD36基因敲除小鼠肌肉和脂肪组织中长链脂肪酸摄取及利用存在缺陷。
J Biol Chem. 2000 Oct 20;275(42):32523-9. doi: 10.1074/jbc.M003826200.
7
Plasma catecholamine and blood lactate responses to incremental arm and leg exercise.血浆儿茶酚胺和血乳酸对递增式手臂和腿部运动的反应。
Med Sci Sports Exerc. 2000 Mar;32(3):608-13. doi: 10.1097/00005768-200003000-00009.
8
Muscle-specific overexpression of FAT/CD36 enhances fatty acid oxidation by contracting muscle, reduces plasma triglycerides and fatty acids, and increases plasma glucose and insulin.FAT/CD36在肌肉中的特异性过表达通过收缩肌肉增强脂肪酸氧化,降低血浆甘油三酯和脂肪酸水平,并提高血浆葡萄糖和胰岛素水平。
J Biol Chem. 1999 Sep 17;274(38):26761-6. doi: 10.1074/jbc.274.38.26761.
9
Expression of hormone-sensitive lipase and its regulation by adrenaline in skeletal muscle.激素敏感性脂肪酶在骨骼肌中的表达及其受肾上腺素的调节
Biochem J. 1999 Jun 1;340 ( Pt 2)(Pt 2):459-65.
10
Identification of Cd36 (Fat) as an insulin-resistance gene causing defective fatty acid and glucose metabolism in hypertensive rats.鉴定Cd36(脂肪)为导致高血压大鼠脂肪酸和葡萄糖代谢缺陷的胰岛素抵抗基因。
Nat Genet. 1999 Jan;21(1):76-83. doi: 10.1038/5013.

CD36缺乏时有氧运动能力减弱。

Attenuated aerobic exercise capacity in CD36 deficiency.

作者信息

Yanai Hidekatsu, Watanabe Ichiro, Ishii Kojiro, Morimoto Mie, Fujiwara Hironobu, Yoshida Shigeru, Hui Shu-Ping, Matsuno Kazuhiko, Chiba Hitoshi

机构信息

Department of Laboratory Medicine, Hokkaido University School of Medicine, Sapporo 060-8648, Japan.

出版信息

J Med Genet. 2007 Jul;44(7):445-7. doi: 10.1136/jmg.2007.050070. Epub 2007 Apr 5.

DOI:10.1136/jmg.2007.050070
PMID:17412877
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2598008/
Abstract

BACKGROUND

An important role of CD36 in muscle fatty acid (FA) uptake has been shown in CD36-knockout or CD36-overexpressed mice. FA is a predominant substrate in energy production during light exercise below the anaerobic threshold (AT). We studied whether aerobic exercise capacity in humans could be affected by CD36 deficiency.

METHODS

We investigated the ventilatory threshold (VT) and serum FA changes in normal participants (n = 22) and participants with CD36 deficiency (n = 12) during pedalling on a cycle ergometer.

RESULTS

In participants with CD36 deficiency, FA levels were not reduced at peak work rate, whereas FA levels decreased by about 50% in normal participants. Participants with CD36 deficiency showed significantly lower VT than normal participants. A significant correlation was observed between VT and percentage changes in FA at peak work rate.

CONCLUSION

This study found reduced FA utilisation and an attenuated aerobic exercise capacity in CD36 deficiency, indicating that CD36-mediated FA oxidation is an important determinant for aerobic exercise capacity in humans.

摘要

背景

在CD36基因敲除或CD36过表达的小鼠中,已证实CD36在肌肉脂肪酸(FA)摄取中起重要作用。在低于无氧阈值(AT)的轻度运动期间,FA是能量产生的主要底物。我们研究了人类的有氧运动能力是否会受到CD36缺乏的影响。

方法

我们调查了正常参与者(n = 22)和CD36缺乏参与者(n = 12)在蹬踩自行车测力计过程中的通气阈值(VT)和血清FA变化。

结果

在CD36缺乏的参与者中,峰值工作率时FA水平未降低,而正常参与者的FA水平下降了约50%。CD36缺乏的参与者的VT显著低于正常参与者。在峰值工作率时,观察到VT与FA百分比变化之间存在显著相关性。

结论

本研究发现CD36缺乏时FA利用减少且有氧运动能力减弱,表明CD36介导的FA氧化是人类有氧运动能力的重要决定因素。