Department of Applied Biological Chemistry, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Tokyo, Japan.
Gen Comp Endocrinol. 2011 Jun 1;172(2):293-304. doi: 10.1016/j.ygcen.2011.03.019. Epub 2011 Apr 5.
Crustacean hyperglycemic hormone (CHH), a member of a neuropeptide family present only in arthropods, plays a pivotal role in the modulation of hemolymph glucose levels, molting, reproduction, and the stress response. Although it has been determined that hepatopancreas and muscle are the major tissues in which CHH regulates hyperglycemic activity, the molecular mechanism by which CHH regulates carbohydrate metabolism remains unclear. In this study, we analyzed the mRNA expression levels of enzymes involved in glycogen metabolism and gluconeogenesis in order to determine how CHH regulates hemolymph glucose levels. We first cloned cDNAs encoding four carbohydrate metabolism-related enzymes from the kuruma prawn, Marsupenaeus japonicus, glycogen phosphorylase (MjGP), glycogen synthase (MjGS), fructose 1,6-bisphosphatase (MjFBPase), and phosphoenolpyruvate carboxykinase (MjPEPCK). RT-PCR analysis showed that eyestalk ablation remarkably decreased MjGP and increased MjGS transcript levels in the hepatopancreas, but not in muscle. Considering the fact that various eyestalk factors, including MIH, are removed by eyestalk ablation, these results indicate that after eyestalk ablation the metabolic state proceeds towards glycogen accumulation in the specific tissues related to molting. In contrast, MjFBPase and MjPEPCK transcript levels were not significantly changed by eyestalk ablation, indicating that CHH and other eyestalk-derived factors might not induce gluconeogenesis. Quantitative real-time PCR analysis showed that exposure of hepatopancreas to recombinant CHH significantly changed the expression levels of MjGP and MjGS, but not MjFBPase and MjPEPCK. Collectively, these results indicate that CHH is involved in glycogen metabolism in hepatopancreas.
甲壳动物血糖激素（CHH）是一种仅存在于节肢动物中的神经肽家族成员，在调节血淋巴葡萄糖水平、蜕皮、繁殖和应激反应中发挥着关键作用。尽管已经确定肝胰腺和肌肉是 CHH 调节高血糖活性的主要组织，但 CHH 调节碳水化合物代谢的分子机制尚不清楚。在本研究中，我们分析了参与糖原代谢和糖异生的酶的 mRNA 表达水平，以确定 CHH 如何调节血淋巴葡萄糖水平。我们首先从日本对虾（Marsupenaeus japonicus）中克隆了与碳水化合物代谢相关的四种酶的 cDNA，即糖原磷酸化酶（MjGP）、糖原合酶（MjGS）、果糖 1,6-二磷酸酶（MjFBPase）和磷酸烯醇丙酮酸羧激酶（MjPEPCK）。RT-PCR 分析表明，眼柄切除显著降低了肝胰腺中 MjGP 的转录水平，增加了 MjGS 的转录水平，但在肌肉中没有。考虑到各种眼柄因子，包括 MIH，都被眼柄切除去除，这些结果表明，眼柄切除后，与蜕皮相关的特定组织中的代谢状态向糖原积累方向发展。相比之下，MjFBPase 和 MjPEPCK 的转录水平并没有因眼柄切除而显著改变，这表明 CHH 和其他眼柄来源的因子可能不会诱导糖异生。定量实时 PCR 分析表明，重组 CHH 暴露于肝胰腺中显著改变了 MjGP 和 MjGS 的表达水平，但 MjFBPase 和 MjPEPCK 的表达水平没有显著改变。总的来说，这些结果表明 CHH 参与了肝胰腺中的糖原代谢。
