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过氧化物酶体增殖剂对肥胖(fa/fa)大鼠β-氧化及整体能量平衡的影响。

Effects of a peroxisome proliferator on beta-oxidation and overall energy balance in obese (fa/fa) rats.

作者信息

Assimacopoulos-Jeannet F, Moinat M, Muzzin P, Colomb C, Jeanrenaud B, Girardier L, Giacobino J P, Seydoux J

机构信息

Laboratoires de Recherches Métaboliques, Geneva, Switzerland.

出版信息

Am J Physiol. 1991 Feb;260(2 Pt 2):R278-83. doi: 10.1152/ajpregu.1991.260.2.R278.

DOI:10.1152/ajpregu.1991.260.2.R278
PMID:1996714
Abstract

The aim of the study was to examine in the obese Zucker (fa/fa) rats the effect of a peroxisome proliferator nafenopin on liver and brown adipose tissue peroxisomal and mitochondrial beta-oxidation enzyme activities and on the overall energy dissipation. A 17-day nafenopin treatment increased liver wet weight 2.1-fold and liver total acyl-CoA oxidase and mitochondria beta-oxidative activities 32- and 4.6-fold, respectively. It increased the interscapular brown adipose tissue (IBAT) acyl-CoA oxidase activity 2.1-fold but had no effect on the mitochondria beta-oxidative activity. Because nafenopin was found to decrease food intake by 22%, obese nafenopin-treated rats were compared with a group of obese pair-fed rats. Both food restriction and nafenopin treatment decreased body weight gain, but a decrease (14%) in fat content was only observed in nafenopin-treated rats. Food restriction of obese rats decreased the mean metabolic rate by 13%, and nafenopin treatment prevented this decrease. Both food restriction and nafenopin treatment decreased the mean daily respiratory quotient (RQ). However, the RQ of nafenopin-treated rats was steadily lower than that of control, whereas that of food-restricted rats was the same as that of control animals during the feeding period and decreased when food supply was exhausted. The increase in liver and IBAT fatty acid beta-oxidative activities may be the cause of the decreased lipid accretion measured in obese rats.

摘要

本研究的目的是检测过氧化物酶体增殖剂萘酚平对肥胖Zucker(fa/fa)大鼠肝脏和棕色脂肪组织中过氧化物酶体及线粒体β-氧化酶活性以及整体能量消耗的影响。为期17天的萘酚平治疗使肝脏湿重增加了2.1倍,肝脏总酰基辅酶A氧化酶和线粒体β-氧化活性分别增加了32倍和4.6倍。它使肩胛间棕色脂肪组织(IBAT)的酰基辅酶A氧化酶活性增加了2.1倍,但对线粒体β-氧化活性没有影响。由于发现萘酚平可使食物摄入量减少22%,因此将接受萘酚平治疗的肥胖大鼠与一组肥胖的配对喂养大鼠进行了比较。食物限制和萘酚平治疗均降低了体重增加,但仅在接受萘酚平治疗的大鼠中观察到脂肪含量下降(14%)。肥胖大鼠的食物限制使平均代谢率降低了13%,而萘酚平治疗可防止这种降低。食物限制和萘酚平治疗均降低了平均每日呼吸商(RQ)。然而,接受萘酚平治疗的大鼠的RQ持续低于对照组,而食物限制大鼠的RQ在喂食期间与对照动物相同,在食物供应耗尽时降低。肝脏和IBAT脂肪酸β-氧化活性的增加可能是肥胖大鼠脂质蓄积减少的原因。

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