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甜菜碱通过调节AMPK/mTOR信号通路改善了投喂高碳水化合物饲料的鳜鱼的食欲调节和糖脂代谢。

Betaine improves appetite regulation and glucose-lipid metabolism in mandarin fish () fed a high-carbohydrate-diet by regulating the AMPK/mTOR signaling.

作者信息

Li Hongyan, Zeng Yanzhi, Wang Guangjun, Zhang Kai, Gong Wangbao, Li Zhifei, Tian Jingjing, Xia Yun, Xie Wenping, Xie Jun, Xie Shouqi, Yu Ermeng

机构信息

Key Laboratory of Tropical & Subtropical Fishery Resource Application & Cultivation, Pearl River Fisheries Research Institute, Chinese Academy of Fishery Sciences, Guangzhou, 510380, China.

Key Laboratory of Breeding Biotechnology and Sustainable Aquaculture, CAS, China.

出版信息

Heliyon. 2024 Mar 30;10(7):e28423. doi: 10.1016/j.heliyon.2024.e28423. eCollection 2024 Apr 15.

DOI:10.1016/j.heliyon.2024.e28423
PMID:38623237
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11016588/
Abstract

Diets with high carbohydrate (HC) was reported to have influence on appetite and intermediary metabolism in fish. To illustrate whether betaine could improve appetite and glucose-lipid metabolism in aquatic animals, mandarin fish () were fed with the HC diets with or without betaine for 8 weeks. The results suggested that betaine enhanced feed intake by regulating the hypothalamic appetite genes. The HC diet-induced downregulation of AMPK and appetite genes was also positively correlated with the decreased autophagy genes, suggesting a possible mechanism that AMPK/mTOR signaling might regulate appetite through autophagy. The HC diet remarkably elevated transcriptional levels of genes related to lipogenesis, while betaine alleviated the HC-induced hepatic lipid deposition. Additionally, betaine supplementation tended to store the energy storage as hepatic glycogen. Our findings proposed the possible mechanism for appetite regulation through autophagy via AMPK/mTOR, and demonstrated the feasibility of betaine as an aquafeed additive to regulate appetite and intermediary metabolism in fish.

摘要

据报道,高碳水化合物(HC)饮食会对鱼类的食欲和中间代谢产生影响。为了阐明甜菜碱是否能改善水生动物的食欲和糖脂代谢,将鳜鱼投喂含或不含甜菜碱的HC饲料8周。结果表明,甜菜碱通过调节下丘脑食欲基因来提高采食量。HC饮食诱导的AMPK和食欲基因下调也与自噬基因的减少呈正相关,提示AMPK/mTOR信号通路可能通过自噬调节食欲的一种潜在机制。HC饮食显著提高了与脂肪生成相关基因的转录水平,而甜菜碱减轻了HC诱导的肝脏脂质沉积。此外,补充甜菜碱倾向于将能量储存为肝糖原。我们的研究结果提出了通过AMPK/mTOR自噬调节食欲的潜在机制,并证明了甜菜碱作为水产饲料添加剂调节鱼类食欲和中间代谢的可行性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1aac/11016588/0c7fa9563884/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1aac/11016588/04fc6849c4fd/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1aac/11016588/d77725369ce1/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1aac/11016588/7be733c10a76/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1aac/11016588/0c7fa9563884/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1aac/11016588/04fc6849c4fd/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1aac/11016588/d77725369ce1/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1aac/11016588/7be733c10a76/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1aac/11016588/0c7fa9563884/gr4.jpg

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