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胆囊收缩素（）在大口黑鲈（）摄食调节中的作用：肽激活与拮抗剂抑制

Role of Cholecystokinin () in Feeding Regulation of Largemouth Bass (): Peptide Activation and Antagonist Inhibition.

作者信息

Liang Hualiang, Mi Haifeng, Yu Heng, Huang Dongyu, Ren Mingchun, Zhang Lu, Teng Tao

机构信息

Key Laboratory of Integrated Rice-Fish Farming Ecology, Ministry of Agriculture and Rural Affairs, Freshwater Fisheries Research Center, Chinese Academy of Fishery Sciences, Wuxi 214081, China.

Tongwei Agricultural Development Co., Ltd., Key Laboratory of Nutrition and Healthy Culture of Aquatic Livestock and Poultry, Ministry of Agriculture and Rural Affairs, Healthy Aquaculture Key Laboratory of Sichuan Province, Chengdu 610093, China.

出版信息

Biology (Basel). 2024 Aug 20;13(8):635. doi: 10.3390/biology13080635.

DOI:10.3390/biology13080635
PMID:39194573
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11351106/
Abstract

This study investigated the role of cholecystokinin () in the feeding regulation of largemouth bass () via peptide activation and antagonist inhibition. The results show that the gene was expressed in various tissues, with the highest expression level occurring in the brain. Feeding, continuous feeding, and refeeding after fasting could significantly improve the mRNA levels of in the brain. Moreover, the activation of via injecting an exogenous CCK peptide could inhibit feed intake by regulating the mRNA levels of anorexigenic and feed-promoting factors in the brain and intestine. Furthermore, the CCK peptide reduced feed intake; however, the presence of an antagonist (Ly225910-CCK1R and devazepide-CCK2R) could reverse this effect through regulating the mRNA levels of anorexigenic and feed-promoting factors in the brain and intestine. Treatment with devazepide + CCK (CCK2R) reversed feed intake more effectively than Ly225910 + CCK (CCK1R) treatment. In summary, could regulate the feed intake of largemouth bass through regulating feeding-related genes in the brain and intestine. In addition, required binding with the receptor to inhibit feed intake more effectively in largemouth bass, and the binding effect of CCK1R was better than that of CCK2R.

摘要

本研究通过肽激活和拮抗剂抑制，探讨了胆囊收缩素（CCK）在大口黑鲈摄食调节中的作用。结果表明，CCK基因在各组织中均有表达，其中在脑中的表达水平最高。摄食、持续投喂以及禁食后的重新投喂均可显著提高脑中CCK的mRNA水平。此外，通过注射外源性CCK肽激活CCK可通过调节脑和肠道中厌食和促摄食因子的mRNA水平来抑制摄食量。此外，CCK肽可降低摄食量；然而，拮抗剂（Ly225910-CCK1R和devazepide-CCK2R）的存在可通过调节脑和肠道中厌食和促摄食因子的mRNA水平来逆转这种作用。用devazepide + CCK（CCK2R）处理比Ly225910 + CCK（CCK1R）处理更有效地逆转了摄食量。总之，CCK可通过调节脑和肠道中与摄食相关的基因来调节大口黑鲈的摄食量。此外，CCK在大口黑鲈中需要与受体结合才能更有效地抑制摄食量，且CCK1R的结合效果优于CCK2R。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/faf8/11351106/59170d8f6273/biology-13-00635-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/faf8/11351106/63c7931d7213/biology-13-00635-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/faf8/11351106/e5f330a12dc0/biology-13-00635-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/faf8/11351106/08dc1e1e3e69/biology-13-00635-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/faf8/11351106/48e81d87f14a/biology-13-00635-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/faf8/11351106/30bc065e7cdc/biology-13-00635-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/faf8/11351106/59170d8f6273/biology-13-00635-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/faf8/11351106/63c7931d7213/biology-13-00635-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/faf8/11351106/e5f330a12dc0/biology-13-00635-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/faf8/11351106/08dc1e1e3e69/biology-13-00635-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/faf8/11351106/48e81d87f14a/biology-13-00635-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/faf8/11351106/30bc065e7cdc/biology-13-00635-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/faf8/11351106/59170d8f6273/biology-13-00635-g006.jpg

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