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新生儿期肝脏脂蛋白脂肪酶表达的消失。

Neonatal extinction of liver lipoprotein lipase expression.

作者信息

Peinado-Onsurbe J, Staels B, Deeb S, Ramirez I, Llobera M, Auwerx J

机构信息

Department of Developmental Biology, University of Leuven, Belgium.

出版信息

Biochim Biophys Acta. 1992 Jul 15;1131(3):281-6. doi: 10.1016/0167-4781(92)90026-v.

DOI:10.1016/0167-4781(92)90026-v
PMID:1627643
Abstract

In contrast to the complete absence of lipoprotein lipase (LPL) mRNA in adult rat liver, fetal and neonatal rat liver contain substantial amounts of LPL mRNA, which is translated in active LPL protein as can be deduced from the presence of LPL activity in this organ. At this neonatal stage, both the relative abundance of LPL mRNA and LPL activity increased with starvation. During the suckling period, LPL mRNA and LPL activity gradually decreased until both parameters were undetectable. While the administration of L-thyroxine or hydrocortisone enhanced the disappearance of LPL mRNA, induced hypothyroidism delayed its disappearance. In adult animals induced hypothyroidism could not reactivate LPL mRNA production in the liver. The data presented suggest that liver LPL production responds to changes in the nutritional state and becomes extinguished during development, in a fashion reminiscent to the extinction of alpha-fetoprotein. This extinction of LPL gene expression is influenced by hormonal factors.

摘要

与成年大鼠肝脏中完全不存在脂蛋白脂肪酶(LPL)mRNA形成对比的是,胎鼠和新生鼠肝脏含有大量LPL mRNA,从该器官中LPL活性的存在可以推断,这些mRNA被翻译为有活性的LPL蛋白。在新生阶段,LPL mRNA的相对丰度和LPL活性都随着饥饿而增加。在哺乳期间,LPL mRNA和LPL活性逐渐降低,直到这两个参数都无法检测到。虽然给予L-甲状腺素或氢化可的松会加速LPL mRNA的消失,但诱导的甲状腺功能减退会延迟其消失。在成年动物中,诱导的甲状腺功能减退不能重新激活肝脏中LPL mRNA的产生。所呈现的数据表明,肝脏LPL的产生对营养状态的变化有反应,并在发育过程中消失,其方式类似于甲胎蛋白的消失。LPL基因表达的这种消失受激素因素影响。

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