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过氧化物酶体增殖但未同时诱导过氧化物酶体脂肪酸β氧化。

Proliferation of peroxisomes without simultaneous induction of the peroxisomal fatty acid beta-oxidation.

作者信息

Baumgart E, Völkl A, Pill J, Fahimi H D

机构信息

Department of Anatomy and Cell Biology II, University of Heidelberg, FRG.

出版信息

FEBS Lett. 1990 May 7;264(1):5-9. doi: 10.1016/0014-5793(90)80750-d.

Abstract

Marked proliferation of rat hepatic peroxisomes is observed after treatment with a new potent hypolipidemic drug BM 15766, as well as after bezafibrate. Whereas the relative specific activity of the peroxisomal fatty acid beta-oxidation system is not affected by BM 15766 it is significantly increased after bezafibrate. This is also confirmed by immunoblot analysis of individual beta-oxidation enzymes in highly purified peroxisome fractions. These observations suggest that peroxisome proliferation and the induction of the fatty acid beta-oxidation are regulated separately.

摘要

用一种新型强效降血脂药物BM 15766治疗后,以及用苯扎贝特治疗后,均可观察到大鼠肝脏过氧化物酶体显著增殖。虽然过氧化物酶体脂肪酸β-氧化系统的相对比活性不受BM 15766影响,但在苯扎贝特治疗后显著增加。这也通过对高度纯化的过氧化物酶体组分中单个β-氧化酶的免疫印迹分析得到证实。这些观察结果表明,过氧化物酶体增殖和脂肪酸β-氧化的诱导是分别调节的。

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