Fatty acid metabolism after short-term fasting: POMC response and EPA signal maintain homeostasis in tilapia.

IF 3.9 2区 医学 Q2 ENDOCRINOLOGY & METABOLISM
Frontiers in Endocrinology Pub Date : 2025-05-09 eCollection Date: 2025-01-01 DOI:10.3389/fendo.2025.1585216
Xiaozheng Yu, Tiansheng Zhu, Yang Yu, Ran Cai, Meiqing Li, Caiyun Sun, Wensheng Li
{"title":"Fatty acid metabolism after short-term fasting: POMC response and EPA signal maintain homeostasis in tilapia.","authors":"Xiaozheng Yu, Tiansheng Zhu, Yang Yu, Ran Cai, Meiqing Li, Caiyun Sun, Wensheng Li","doi":"10.3389/fendo.2025.1585216","DOIUrl":null,"url":null,"abstract":"<p><p>Detecting and responding to fluctuations in fatty acid levels is crucial for maintaining the homeostasis of fatty acid metabolism. This study examined changes in neuropeptide levels and fatty acid sensing systems in tilapia following 24-hour fasting. Subsequently, an EPA compensation experiment was conducted to examine the regulatory effects of hypothalamic neuropeptides on feeding activity, fatty acid sensing systems activation, and alterations in AMPK and AKT signaling pathways in tilapia. After fasting, the neuropeptide Y signals in the preglomerular nucleus region increased significantly, while the POMC in the lateral tuberal nucleus significantly decreased. There was a significant increase in most long-chain fatty acids, excluding the EPA which declined. Fasting activates fatty acid sensing systems regulated by fatty acid metabolism and mitochondrial activity in the hypothalamus, and those regulated by CD36, mitochondrial activity and PKC in the liver. However, it inhibited systems regulated by fatty acid metabolism and lipoprotein lipase in the liver. Intraperitoneal EPA injection raised <i>pomc</i> mRNA levels in the hypothalamus after short-term fasting and curtailed food intake. EPA compensation inhibited the liver fatty acid metabolism, CD36, and mitochondrial activity-related fatty acid sensing systems, and lipoprotein lipase-regulated fatty acid sensing systems in the hypothalamus while activating lipoprotein lipase-regulated fatty acid sensing systems in the liver. Moreover, EPA suppressed the AMPK pathway in both tissues. Following fasting, serum EPA levels decreased, accompanied by lower POMC in the brain and activation of the fatty acid sensing systems in hypothalamus and liver. EPA compensation inhibited the AMPK pathway, increased <i>pomc</i> mRNA in the hypothalamus and suppressed food intake as a satiation factor. This research offers insights into how the central nervous system and peripheral tissues respond to fatty acid levels during hunger in tilapia.</p>","PeriodicalId":12447,"journal":{"name":"Frontiers in Endocrinology","volume":"16 ","pages":"1585216"},"PeriodicalIF":3.9000,"publicationDate":"2025-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12098032/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Frontiers in Endocrinology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.3389/fendo.2025.1585216","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/1 0:00:00","PubModel":"eCollection","JCR":"Q2","JCRName":"ENDOCRINOLOGY & METABOLISM","Score":null,"Total":0}
引用次数: 0

Abstract

Detecting and responding to fluctuations in fatty acid levels is crucial for maintaining the homeostasis of fatty acid metabolism. This study examined changes in neuropeptide levels and fatty acid sensing systems in tilapia following 24-hour fasting. Subsequently, an EPA compensation experiment was conducted to examine the regulatory effects of hypothalamic neuropeptides on feeding activity, fatty acid sensing systems activation, and alterations in AMPK and AKT signaling pathways in tilapia. After fasting, the neuropeptide Y signals in the preglomerular nucleus region increased significantly, while the POMC in the lateral tuberal nucleus significantly decreased. There was a significant increase in most long-chain fatty acids, excluding the EPA which declined. Fasting activates fatty acid sensing systems regulated by fatty acid metabolism and mitochondrial activity in the hypothalamus, and those regulated by CD36, mitochondrial activity and PKC in the liver. However, it inhibited systems regulated by fatty acid metabolism and lipoprotein lipase in the liver. Intraperitoneal EPA injection raised pomc mRNA levels in the hypothalamus after short-term fasting and curtailed food intake. EPA compensation inhibited the liver fatty acid metabolism, CD36, and mitochondrial activity-related fatty acid sensing systems, and lipoprotein lipase-regulated fatty acid sensing systems in the hypothalamus while activating lipoprotein lipase-regulated fatty acid sensing systems in the liver. Moreover, EPA suppressed the AMPK pathway in both tissues. Following fasting, serum EPA levels decreased, accompanied by lower POMC in the brain and activation of the fatty acid sensing systems in hypothalamus and liver. EPA compensation inhibited the AMPK pathway, increased pomc mRNA in the hypothalamus and suppressed food intake as a satiation factor. This research offers insights into how the central nervous system and peripheral tissues respond to fatty acid levels during hunger in tilapia.

短期禁食后脂肪酸代谢:POMC反应和EPA信号维持罗非鱼体内稳态。
检测和响应脂肪酸水平的波动对于维持脂肪酸代谢的稳态至关重要。本研究检测了罗非鱼禁食24小时后神经肽水平和脂肪酸感应系统的变化。随后,进行了EPA补偿实验,以研究下丘脑神经肽对罗非鱼摄食活性、脂肪酸传感系统激活以及AMPK和AKT信号通路改变的调节作用。禁食后,肾小球前核区神经肽Y信号明显升高,结节外侧核区POMC明显降低。除EPA下降外,大部分长链脂肪酸显著增加。禁食激活由下丘脑脂肪酸代谢和线粒体活性调节的脂肪酸传感系统,以及由肝脏CD36、线粒体活性和PKC调节的系统。然而,它抑制了肝脏中脂肪酸代谢和脂蛋白脂肪酶调节的系统。短期禁食和减少食物摄入后,腹腔注射EPA可提高下丘脑pomc mRNA水平。EPA补偿抑制肝脏脂肪酸代谢、CD36、线粒体活性相关的脂肪酸传感系统和下丘脑脂蛋白脂酶调节的脂肪酸传感系统,同时激活肝脏脂蛋白脂酶调节的脂肪酸传感系统。此外,EPA在两种组织中均抑制AMPK通路。禁食后,血清EPA水平下降,大脑中POMC降低,下丘脑和肝脏中脂肪酸感知系统激活。EPA补偿抑制了AMPK途径,增加了下丘脑的pomc mRNA,并抑制了作为饱足因子的食物摄入。这项研究为罗非鱼在饥饿期间中枢神经系统和外周组织如何对脂肪酸水平做出反应提供了见解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
Frontiers in Endocrinology
Frontiers in Endocrinology Medicine-Endocrinology, Diabetes and Metabolism
CiteScore
5.70
自引率
9.60%
发文量
3023
审稿时长
14 weeks
期刊介绍: Frontiers in Endocrinology is a field journal of the "Frontiers in" journal series. In today’s world, endocrinology is becoming increasingly important as it underlies many of the challenges societies face - from obesity and diabetes to reproduction, population control and aging. Endocrinology covers a broad field from basic molecular and cellular communication through to clinical care and some of the most crucial public health issues. The journal, thus, welcomes outstanding contributions in any domain of endocrinology. Frontiers in Endocrinology publishes articles on the most outstanding discoveries across a wide research spectrum of Endocrinology. The mission of Frontiers in Endocrinology is to bring all relevant Endocrinology areas together on a single platform.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信