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草鱼GIPR的分子特征以及营养状态、胰岛素和胰高血糖素对其表达的影响

Molecular Characterization of Grass Carp GIPR and Effect of Nutrition States, Insulin, and Glucagon on Its Expression.

作者信息

Yang Guokun, Liang Xiaomin, Jiang Yanle, Li Chengquan, Zhang Yanmin, Zhang Xindang, Chang Xulu, Shen Yawei, Meng Xiaolin

机构信息

College of Fisheries, Henan Normal University, Xinxiang 453007, China.

Engineering Technology Research Center of Henan Province for Aquatic Animal Cultivation, Henan Normal University, Xinxiang 453007, China.

出版信息

Aquac Nutr. 2022 Nov 7;2022:4330251. doi: 10.1155/2022/4330251. eCollection 2022.

DOI:10.1155/2022/4330251
PMID:36860432
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9973162/
Abstract

GIP plays an important regulatory role in glucose and lipid metabolism. As the specific receptor, GIPR is involved in this physiological process. To assess the roles of GIPR in teleost, the GIPR gene was cloned from grass carp. The ORF of cloned GIPR gene was 1560 bp, encoding 519 amino acids. The grass carp GIPR was the G-protein-coupled receptor which contains seven predicted transmembrane domains. In addition, two predicted glycosylation sites were contained in the grass carp GIPR. The grass carp GIPR expression is in multiple tissues and is highly expressed in the kidney, brain regions, and visceral fat tissue. In the OGTT experiment, the GIPR expression is markedly decreased in the kidney, visceral fat, and brain by treatment with glucose for 1 and 3 h. In the fast and refeeding experiment, the GIPR expression in the kidney and visceral fat tissue was significantly induced in the fast groups. In addition, the GIPR expression levels were markedly decreased in the refeeding groups. In the present study, the visceral fat accumulation of grass carp was induced by overfed. The GIPR expression was significantly decreased in the brain, kidney, and visceral fat tissue of overfed grass carp. In primary hepatocytes, the GIPR expression was promoted by treatment with oleic acid and insulin. The GIPR mRNA levels were significantly reduced by treatment with glucose and glucagon in the grass carp primary hepatocytes. To our knowledge, this is the first time the biological role of GIPR is unveiled in teleost.

摘要

胃抑制多肽(GIP)在葡萄糖和脂质代谢中发挥着重要的调节作用。作为特异性受体,GIP受体(GIPR)参与了这一生理过程。为了评估GIPR在硬骨鱼中的作用,从草鱼中克隆了GIPR基因。克隆的GIPR基因的开放阅读框(ORF)为1560 bp,编码519个氨基酸。草鱼GIPR是一种G蛋白偶联受体,含有7个预测的跨膜结构域。此外,草鱼GIPR中含有两个预测的糖基化位点。草鱼GIPR在多个组织中表达,在肾脏、脑区和内脏脂肪组织中高表达。在口服葡萄糖耐量试验(OGTT)中,用葡萄糖处理1小时和3小时后,肾脏、内脏脂肪和脑中的GIPR表达明显降低。在禁食和再投喂实验中,禁食组肾脏和内脏脂肪组织中的GIPR表达显著诱导。此外,再投喂组中的GIPR表达水平明显降低。在本研究中,过度投喂诱导了草鱼内脏脂肪的积累。过度投喂的草鱼脑、肾和内脏脂肪组织中的GIPR表达显著降低。在原代肝细胞中,油酸和胰岛素处理可促进GIPR表达。在草鱼原代肝细胞中,葡萄糖和胰高血糖素处理可显著降低GIPR mRNA水平。据我们所知,这是首次在硬骨鱼中揭示GIPR的生物学作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c252/9973162/425c7529e30e/ANU2022-4330251.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c252/9973162/b26a95814bd8/ANU2022-4330251.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c252/9973162/03ebfb90e0e0/ANU2022-4330251.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c252/9973162/c7a5326388dc/ANU2022-4330251.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c252/9973162/16b71483c458/ANU2022-4330251.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c252/9973162/ec7642a0fade/ANU2022-4330251.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c252/9973162/425c7529e30e/ANU2022-4330251.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c252/9973162/b26a95814bd8/ANU2022-4330251.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c252/9973162/03ebfb90e0e0/ANU2022-4330251.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c252/9973162/c7a5326388dc/ANU2022-4330251.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c252/9973162/16b71483c458/ANU2022-4330251.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c252/9973162/ec7642a0fade/ANU2022-4330251.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c252/9973162/425c7529e30e/ANU2022-4330251.006.jpg

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Targeting the GIPR for obesity: To agonize or antagonize? Potential mechanisms.针对肥胖的 GIPR 靶点:激动还是拮抗?潜在机制。
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The gut hormone receptor GIPR links energy availability to the control of hematopoiesis.肠道激素受体 GIPR 将能量可用性与造血控制联系起来。
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Pharmacological antagonism of the incretin system protects against diet-induced obesity.肠促胰岛素系统的药理学拮抗作用可预防饮食诱导的肥胖。
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