Comparative effect of fenofibrate on hepatic desaturases in wild-type and peroxisome proliferator-activated receptor α-deficient mice
Comparative effect of fenofibrate on hepatic desaturases in wild-type and peroxisome proliferator-activated receptor α-deficient mice
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DOI：
10.1007/s11745-006-0990-3
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发表时间：
2002-10-01
期刊：
影响因子：
1.9
通讯作者：
Legrand, P
中科院分区：
文献类型：
--
作者：
Guillou, H;Martin, P;Legrand, P
在这项研究中，提出了非诺贝特，一个原型的过氧化物酶体增殖物的贝特类，野生型和过氧化物酶体增殖物激活受体α（PPARalpha）-/-小鼠肝脏FA谱，去饱和酶mRNA水平和活动的影响。我们确定，过氧化物酶体增殖物暴露后，肝脏FA的配置文件被大大修改。肝脏FA含量的这些改变需要PPARalpha的表达，因为它们在这种核受体缺陷的转基因小鼠中受到抑制。暴露于过氧化物酶体增殖物后，野生型小鼠肝脏中Delta 6和Delta 5去饱和酶mRNA水平和活性增加，但PPARalpha缺陷小鼠肝脏中则没有增加。这些结果表明PPARa参与了小鼠肝Δ 6-和Δ 5-去饱和酶的控制。他们的作用，最大限度地减少长链PUFA消耗在肝脏过氧化物酶体增殖剂暴露过程中进行了讨论。
In this study is presented the effect of fenofibrate, a prototypical peroxisome proliferator of the fibrate class, on wild-type and peroxisome proliferator-activated receptor cc (PPARalpha)-/- mouse liver FA profile, desaturase mRNA levels, and activities. We established that, following peroxisome proliferator exposure, the hepatic FA profile was greatly modified. These modifications in hepatic FA content required the expression of PPARalpha, as they are suppressed in transgenic mice deficient in this nuclear receptor. Following peroxisome proliferator exposure, Delta6- and Delta5-desaturase mRNA levels and activities were increased in wild-type but not in PPARalpha-deficient mouse liver. These results suggest the involvement of PPARa in the control of hepatic Delta6- and Delta5-desaturases in mice. Their roles in minimizing long-chain PUFA depletion in the liver during peroxisome proliferator exposure are discussed.