Expression of insulin-like growth factors at mRNA levels during the metamorphic development of turbot (Scophthalmus maximus)

文献类型： 外文期刊

第一作者： Meng, Zhen

作者： Meng, Zhen;Hu, Peng;Lei, Jilin;Jia, Yudong

作者机构：

关键词： IGF-I; IGF-II; Metamorphosis; Turbot (Scophthalmus maximus)

期刊名称：GENERAL AND COMPARATIVE ENDOCRINOLOGY （ 影响因子：2.822； 五年影响因子：2.772 ）

ISSN： 0016-6480

年卷期： 2016 年 235 卷

页码：

收录情况： SCI

摘要： Insulin-like growth factors I and H (IGF-I and IGF-II) are important regulators of vertebrate growth and development. This study characterized the mRNA expressions of igf-i and igf-ii during turbot (Scophthalmus maximus) metamorphosis to elucidate the possible regulatory role of the IGF system in flatfish metamorphosis. Results showed that the mRNA levels of igf-i significantly increased at the early-metamorphosis stage and then gradually decreased until metamorphosis was completed. By contrast, mRNA levels of igf-ii significantly increased at the pre-metamorphosis stage and then substantially decreased during metamorphosis. Meanwhile, the whole-body thyroxine (T4) levels varied during larval metamorphosis, and the highest value was observed in the Climax-metamorphosis. The mRNA levels of igf-i significantly increased and decreased by T4 and thiourea (TU, inhibitor of endogenous thyroid hormone) during metamorphosis, respectively. Conversely, the mRNA levels of igf-ii remained unchanged. Furthermore, TU significantly inhibited the T4-induced mRNA up-regulation of igf-i during metamorphosis. The whole-body thyroxine (T4) levels were significantly increased and decreased by T4 and TU during metamorphosis, respectively. These results suggested that igf-i and igf-ii may play different functional roles in larval development stages, and igf-i may have a crucial function in regulating the early metamorphic development of turbot. These findings may enhance our understanding of the potential roles of the IGF system to control flatfish metamorphosis and contribute to the improvement of broodstock management for larvae. (C) 2016 Published by Elsevier Inc.

分类号：

  • 相关文献
作者其他论文 更多>>

微信小程序