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胰岛素样肽 1(DILP1)在幼虫和成虫阶段的代谢中的调节作用不同。

Regulatory Roles of Insulin-Like Peptide 1 (DILP1) in Metabolism Differ in Pupal and Adult Stages.

机构信息

Department of Zoology, Stockholm University, Stockholm, Sweden.

Department of Ecology and Evolutionary Biology, Brown University, Providence, RI, United States.

出版信息

Front Endocrinol (Lausanne). 2020 Apr 21;11:180. doi: 10.3389/fendo.2020.00180. eCollection 2020.

DOI:10.3389/fendo.2020.00180
PMID:32373064
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7186318/
Abstract

The insulin/IGF-signaling pathway is central in control of nutrient-dependent growth during development, and in adult physiology and longevity. Eight insulin-like peptides (DILP1-8) have been identified in , and several of these are known to regulate growth, metabolism, reproduction, stress responses, and lifespan. However, the functional role of DILP1 is far from understood. Previous work has shown that /DILP1 is transiently expressed mainly during the pupal stage and the first days of adult life. Here, we study the role of in the pupa, as well as in the first week of adult life, and make some comparisons to that displays a similar pupal expression profile, but is expressed in fat body rather than brain neurosecretory cells. We show that mutation of diminishes organismal weight during pupal development, whereas overexpression increases it, similar to manipulations. No growth effects of or manipulations were detected during larval development. We next show that and increase metabolic rate in the late pupa and promote lipids as the primary source of catabolic energy. Effects of manipulations can also be seen in the adult fly. In newly eclosed female flies, survival during starvation is strongly diminished in mutants, but not in and / mutants, whereas in older flies, only the double mutants display reduced starvation resistance. Starvation resistance is not affected in male mutant flies, suggesting a sex dimorphism in function. Overexpression of also decreases survival during starvation in female flies and increases egg laying and decreases egg to pupal viability. In conclusion, and overexpression promotes metabolism and growth of adult tissues during the pupal stage, likely by utilization of stored lipids. Some of the effects of the manipulations may carry over from the pupa to affect physiology in young adults, but our data also suggest that signaling is important in metabolism and stress resistance in the adult stage.

摘要

胰岛素/IGF 信号通路是控制发育过程中营养依赖型生长以及成年生理和寿命的核心。在 中已鉴定出 8 种胰岛素样肽 (DILP1-8),其中一些已知可调节生长、代谢、繁殖、应激反应和寿命。然而,DILP1 的功能作用还远未被理解。先前的工作表明,/DILP1 在蛹期和成年后的最初几天主要是短暂表达的。在这里,我们研究了 在蛹期以及成年后的第一周的作用,并与 /DILP1 进行了一些比较,后者表现出相似的蛹期表达模式,但在脂肪体中表达而不是在脑神经分泌细胞中表达。我们表明,/的突变会在蛹期发育过程中减少生物体的重量,而过表达则会增加其重量,这与 /的操作相似。在幼虫发育过程中,/或 /的操作没有检测到生长影响。我们接下来表明,/和 /在晚期蛹中增加代谢率,并促进脂质作为主要的分解能量来源。/操作的影响也可以在成年果蝇中看到。在刚羽化的雌性果蝇中,饥饿条件下的存活率在 /突变体中大大降低,但在 /和 /突变体中则没有,而在较老的果蝇中,只有双突变体显示出降低的饥饿抗性。在雄性 /突变体果蝇中,饥饿抗性不受影响,这表明 /功能存在性别二态性。/的过表达也会降低雌性果蝇在饥饿条件下的存活率,并增加产卵量和降低卵到蛹的存活率。总之,/和 /的过表达促进了蛹期成年组织的代谢和生长,可能通过利用储存的脂质来实现。/操作的一些影响可能会从蛹期延续到影响年轻成年期的生理机能,但我们的数据也表明,/信号在成年期的代谢和应激抗性中很重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9049/7186318/7fb0047978ad/fendo-11-00180-g0008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9049/7186318/fb89b58bda3d/fendo-11-00180-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9049/7186318/e1d8a2167d63/fendo-11-00180-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9049/7186318/dff6071c1104/fendo-11-00180-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9049/7186318/292b82e8b4e3/fendo-11-00180-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9049/7186318/78e7df92bb09/fendo-11-00180-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9049/7186318/b9256b5475ad/fendo-11-00180-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9049/7186318/5b88f77d5ebc/fendo-11-00180-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9049/7186318/7fb0047978ad/fendo-11-00180-g0008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9049/7186318/fb89b58bda3d/fendo-11-00180-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9049/7186318/e1d8a2167d63/fendo-11-00180-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9049/7186318/dff6071c1104/fendo-11-00180-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9049/7186318/292b82e8b4e3/fendo-11-00180-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9049/7186318/78e7df92bb09/fendo-11-00180-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9049/7186318/b9256b5475ad/fendo-11-00180-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9049/7186318/5b88f77d5ebc/fendo-11-00180-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9049/7186318/7fb0047978ad/fendo-11-00180-g0008.jpg

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