食欲调节肽Ghrelin和GLP-1与酒精使用障碍的关系

4区 医学 Q2 Biochemistry, Genetics and Molecular Biology
Elisabet Jerlhag
{"title":"食欲调节肽Ghrelin和GLP-1与酒精使用障碍的关系","authors":"Elisabet Jerlhag","doi":"10.1007/978-3-031-89525-8_8","DOIUrl":null,"url":null,"abstract":"<p><p>The body-brain connection is well-established, further evidenced by studies on the orexigenic peptide ghrelin and the anorexigenic peptide glucagon-like peptide-1 (GLP-1). The ghrelin pathway consists of several substrates, which has been studied in relation to alcohol-related responses. Preclinical studies have found that central ghrelin infusions elevate alcohol intake, whereas suppression of the ghrelin receptors (GHSR) attenuates alcohol-related responses. On a similar note, the endogenous GHSR inverse agonist, LEAP2, and the precursor of ghrelin, DAG, block the stimulatory properties of alcohol and reduce alcohol intake. GLP-1 receptor agonists are currently approved for the treatment of type 2 diabetes and obesity. Recent advances in rodents have extended the pharmacological relevance of these GLP-1 receptor agonists as they mitigate alcohol-related responses. Specifically, in animal models reflecting alcohol use disorder (AUD) all tested GLP-1 receptor agonists reduce alcohol intake, suppress the motivation to consume alcohol, and prevent relapse drinking, effects most likely driven by an attenuation of alcohol-induced reward. Additional experiments were conducted in attempts to define areas and circuits responsible for ghrelin and GLP-1 to control alcohol-related responses. Specifically, areas associated with reward were defined as important modulatory areas. In summary, the ghrelin pathway and GLP-1 participate in the pathophysiology of AUD, thereby providing tentative treatment targets.</p>","PeriodicalId":7270,"journal":{"name":"Advances in experimental medicine and biology","volume":"1477 ","pages":"229-241"},"PeriodicalIF":0.0000,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"The Connection Between the Appetite-Regulatory Peptides Ghrelin and GLP-1 and Alcohol Use Disorder.\",\"authors\":\"Elisabet Jerlhag\",\"doi\":\"10.1007/978-3-031-89525-8_8\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>The body-brain connection is well-established, further evidenced by studies on the orexigenic peptide ghrelin and the anorexigenic peptide glucagon-like peptide-1 (GLP-1). The ghrelin pathway consists of several substrates, which has been studied in relation to alcohol-related responses. Preclinical studies have found that central ghrelin infusions elevate alcohol intake, whereas suppression of the ghrelin receptors (GHSR) attenuates alcohol-related responses. On a similar note, the endogenous GHSR inverse agonist, LEAP2, and the precursor of ghrelin, DAG, block the stimulatory properties of alcohol and reduce alcohol intake. GLP-1 receptor agonists are currently approved for the treatment of type 2 diabetes and obesity. Recent advances in rodents have extended the pharmacological relevance of these GLP-1 receptor agonists as they mitigate alcohol-related responses. Specifically, in animal models reflecting alcohol use disorder (AUD) all tested GLP-1 receptor agonists reduce alcohol intake, suppress the motivation to consume alcohol, and prevent relapse drinking, effects most likely driven by an attenuation of alcohol-induced reward. Additional experiments were conducted in attempts to define areas and circuits responsible for ghrelin and GLP-1 to control alcohol-related responses. Specifically, areas associated with reward were defined as important modulatory areas. In summary, the ghrelin pathway and GLP-1 participate in the pathophysiology of AUD, thereby providing tentative treatment targets.</p>\",\"PeriodicalId\":7270,\"journal\":{\"name\":\"Advances in experimental medicine and biology\",\"volume\":\"1477 \",\"pages\":\"229-241\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2025-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Advances in experimental medicine and biology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1007/978-3-031-89525-8_8\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"Biochemistry, Genetics and Molecular Biology\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Advances in experimental medicine and biology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/978-3-031-89525-8_8","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"Biochemistry, Genetics and Molecular Biology","Score":null,"Total":0}
引用次数: 0

摘要

体脑之间的联系已被证实,对厌氧肽ghrelin和厌氧肽胰高血糖素样肽-1 (GLP-1)的研究进一步证明了这一点。胃饥饿素途径由几种底物组成,这些底物与酒精相关的反应有关。临床前研究发现,中枢胃饥饿素输注会增加酒精摄入量,而抑制胃饥饿素受体(GHSR)则会减弱酒精相关反应。同样,内源性GHSR逆激动剂LEAP2和胃饥饿素前体DAG可阻断酒精的刺激特性并减少酒精摄入量。GLP-1受体激动剂目前被批准用于治疗2型糖尿病和肥胖症。最近啮齿动物的研究进展扩展了这些GLP-1受体激动剂的药理学相关性,因为它们减轻了酒精相关的反应。具体来说,在反映酒精使用障碍(AUD)的动物模型中,所有测试的GLP-1受体激动剂都能减少酒精摄入量,抑制饮酒动机,防止饮酒复发,这些效果很可能是由酒精诱导的奖励衰减驱动的。他们还进行了其他实验,试图确定负责胃饥饿素和GLP-1的区域和回路,以控制与酒精相关的反应。具体来说,与奖励相关的区域被定义为重要的调节区域。综上所述,ghrelin通路和GLP-1参与AUD的病理生理,从而提供了初步的治疗靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The Connection Between the Appetite-Regulatory Peptides Ghrelin and GLP-1 and Alcohol Use Disorder.

The body-brain connection is well-established, further evidenced by studies on the orexigenic peptide ghrelin and the anorexigenic peptide glucagon-like peptide-1 (GLP-1). The ghrelin pathway consists of several substrates, which has been studied in relation to alcohol-related responses. Preclinical studies have found that central ghrelin infusions elevate alcohol intake, whereas suppression of the ghrelin receptors (GHSR) attenuates alcohol-related responses. On a similar note, the endogenous GHSR inverse agonist, LEAP2, and the precursor of ghrelin, DAG, block the stimulatory properties of alcohol and reduce alcohol intake. GLP-1 receptor agonists are currently approved for the treatment of type 2 diabetes and obesity. Recent advances in rodents have extended the pharmacological relevance of these GLP-1 receptor agonists as they mitigate alcohol-related responses. Specifically, in animal models reflecting alcohol use disorder (AUD) all tested GLP-1 receptor agonists reduce alcohol intake, suppress the motivation to consume alcohol, and prevent relapse drinking, effects most likely driven by an attenuation of alcohol-induced reward. Additional experiments were conducted in attempts to define areas and circuits responsible for ghrelin and GLP-1 to control alcohol-related responses. Specifically, areas associated with reward were defined as important modulatory areas. In summary, the ghrelin pathway and GLP-1 participate in the pathophysiology of AUD, thereby providing tentative treatment targets.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Advances in experimental medicine and biology
Advances in experimental medicine and biology 医学-医学:研究与实验
CiteScore
5.90
自引率
0.00%
发文量
465
审稿时长
2-4 weeks
期刊介绍: Advances in Experimental Medicine and Biology provides a platform for scientific contributions in the main disciplines of the biomedicine and the life sciences. This series publishes thematic volumes on contemporary research in the areas of microbiology, immunology, neurosciences, biochemistry, biomedical engineering, genetics, physiology, and cancer research. Covering emerging topics and techniques in basic and clinical science, it brings together clinicians and researchers from various fields.
×
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:604180095
Book学术官方微信