As ligands of the sugar gustatory receptors, sugars have been known to activate the insulin/insulin-like growth factor signaling pathway; however, the precise pathways that are activated by the sugar-bound gustatory receptors in insects remain unclear. In this study, we aimed to investigate the signaling cascades activated by NlGr11, a sugar gustatory receptor in the brown planthopper Nilaparvata lugens (Stål), and its ligand. Galactose-bound NlGr11 (galactose-NlGr11) activated the -phosphatidylinositol 3-kinase (PI3K)-AKT signaling cascade via insulin receptor (InR) and Gβγ in vitro. In addition, galactose-NlGr11 inhibited the AMP-activated protein kinase (AMPK) phosphorylation by activating the AKT-phosphofructokinase (PFK)-ATP signaling cascade in vitro. Importantly, the InR-PI3K-AKT-PFK-AKT signaling cascade was activated and the AMPK phosphorylation was inhibited after feeding the brown planthoppers with galactose solution. Collectively, these findings confirm that NlGr11 can inhibit AMPK phosphorylation by activating the PI3K-AKT-PFK-ATP signaling cascades via both the InR and Gβγ when bound to galactose. Thus, our study provides novel insights into the signaling pathways regulated by the sugar gustatory receptors in insects. This article is protected by copyright. All rights reserved.

中文翻译：

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半乳糖-Nl Gr11 通过胰岛素受体和 Gβγ 激活 PI3K-AKT-PKF-ATP 信号级联反应抑制 AMPK 磷酸化

作为糖味受体的配体，已知糖可以激活胰岛素/胰岛素样生长因子信号通路；然而，昆虫中糖结合味觉受体激活的精确途径仍不清楚。在这项研究中，我们旨在研究 NlGr11 激活的信号级联反应，NlGr11 是褐飞虱 Nilaparvata lugens (Stål) 中的糖味受体及其配体。半乳糖结合的 NlGr11（半乳糖-NlGr11）在体外通过胰岛素受体 (InR) 和 Gβγ 激活了 β-磷脂酰肌醇 3-激酶 (PI3K)-AKT 信号级联反应。此外，半乳糖-NlGr11 通过在体外激活 AKT-磷酸果糖激酶 (PFK)-ATP 信号级联反应来抑制 AMP 活化蛋白激酶 (AMPK) 磷酸化。重要的，在用半乳糖溶液喂养褐飞虱后，InR-PI3K-AKT-PFK-AKT 信号级联被激活，AMPK 磷酸化被抑制。总的来说，这些发现证实 NlGr11 可以通过与半乳糖结合时通过 InR 和 Gβγ 激活 PI3K-AKT-PFK-ATP 信号级联来抑制 AMPK 磷酸化。因此，我们的研究为昆虫中糖味受体调节的信号通路提供了新的见解。本文受版权保护。版权所有。我们的研究为昆虫中糖味受体调节的信号通路提供了新的见解。本文受版权保护。版权所有。我们的研究为昆虫中糖味受体调节的信号通路提供了新的见解。本文受版权保护。版权所有。