在昆虫中，蜕皮激素（20E）通过诱导蜕皮和变态决定个体生长时间；而胰岛素信号则调控个体生长速率；20E和胰岛素信号共同决定个体大小。我们还发现，20E可以在果蝇脂肪体中激活AMPK-PP2A以拮抗胰岛素信号和抑制个体生长速率（PNAS，2020）；初步结果显示，脂肪体胰岛素信号能够促进摄食和提高个体生长速率，具体机理还不清楚。本项目拟结合组学和果蝇遗传学阐明脂肪体胰岛素信号影响昆虫摄食行为的分子机理。首先，通过转录组-代谢组关联分析解答脂肪体胰岛素信号促进摄食的可能机理；然后，结合组学结果，筛选与摄食相关的胰岛素信号下游基因和脂肪体分泌因子，并进行摄食相关功能验证；最后，对脑和中肠进行转录组分析和功能验证，鉴定受脂肪体分泌因子作用的、调控昆虫摄食行为的神经肽或神经递质信号通路。该研究将解析果蝇脂肪体胰岛素信号促进摄食和调控个体生长速率的分子机理，为高等动物个体大小的调控机制提供理论依据。

In insects, the steroid hormone 20-hydroxyecdysone (20E) and insulin/IGF signaling (IIS) are mainly responsible for the growth rate and growth period, respectively, consequently the final body size. 20E restricts the growth period by triggering developmental transitions; while IIS regulates the growth rate. We previously found that 20E antagonizes IIS through the AMPK-PP2A axis in the fat body and suppressed the growth rate (PNAS, 2020). Preliminary results show that IIS in the fat body can promote food consumption and growth rate, the molecular mechanism is still unclear. This project intends to clarify the molecular mechanism of IIS in fat body influencing insect feeding behavior in combination with omics and Drosophila genetics. First, this project will analyze the possible mechanism of IIS promoting food intake in the fat body through the transcriptome-metabolic association analysis. Then, with the results of omics analysis, we will screen out downstream genes of IIS and fat body secretory factors related to food intake, and perform food intake related function verification. Finally, transcriptome analysis and functional verification of the brain and midgut will be performed to identify neuropeptide or neurotransmitter signaling pathways which affected by the fat body secretory factors and regulate insect feeding behavior. This study will analyze the molecular mechanism of IIS in the fat body of Drosophila promote food consumption and growth rate, and provide a theoretical basis for the regulation mechanism of individual size of higher animals.