胰高血糖素样肽-1和趋化素在肥胖发展中的相反作用的研究进展。

IF 2.8 4区 医学 Q2 MEDICINE, RESEARCH & EXPERIMENTAL Experimental Biology and Medicine Pub Date : 2023-11-01 Epub Date: 2023-12-06 DOI:10.1177/15353702231214270
Qilong Zhang, Jianping Ye, Xiaohui Wang
{"title":"胰高血糖素样肽-1和趋化素在肥胖发展中的相反作用的研究进展。","authors":"Qilong Zhang, Jianping Ye, Xiaohui Wang","doi":"10.1177/15353702231214270","DOIUrl":null,"url":null,"abstract":"<p><p>Glucagon-like peptide-1 (GLP-1), secreted by intestinal L-cells, plays a pivotal role in the modulation of β-cell insulin secretion in a glucose-dependent manner, concurrently promoting β-cell survival and β-cell mass. Notably, GLP-1 has emerged as an effective second-line treatment for type 2 diabetes mellitus, gaining further prominence for its pronounced impact on body weight reduction, positioning it as a potent antiobesity agent. However, the mechanism by which GLP-1 improves obesity remains unclear. Some reports suggest that this mechanism may be associated with the regulation of adipokine synthesis within adipose tissue. Chemerin, a multifunctional adipokine and chemokine, has been identified as a pivotal player in adipocyte differentiation and the propagation of systemic inflammation, a hallmark of obesity. This review provides a comprehensive overview of the mechanisms by which GLP-1 and chemerin play crucial roles in obesity and obesity-related diseases. It discusses well-established aspects, such as their effects on food intake and glycolipid metabolism, as well as recent insights, including their influence on macrophage polarization and adipose tissue thermogenesis. GLP-1 has been shown to increase the population of anti-inflammatory M2 macrophages, promote brown adipose tissue thermogenesis, and induce the browning of white adipose tissue. In contrast, chemerin exhibits opposite effects in these processes. In addition, recent research findings have demonstrated the promising potential of GLP-1-based therapies in directly or indirectly regulating chemerin expression. In an intriguing reciprocal relationship, chemerin has also been newly identified as a negative regulator of GLP-1 <i>in vivo</i>. This review delineates the intricate interplay between GLP-1 and chemerin, unraveling their mutual inhibitory interactions. To the best of our knowledge, no previous reviews have focused on this specific topic, making this review particularly valuable in expanding our understanding of the endocrine mechanisms of obesity and providing potential strategies for the treatment of obesity and related diseases.</p>","PeriodicalId":12163,"journal":{"name":"Experimental Biology and Medicine","volume":" ","pages":"2020-2029"},"PeriodicalIF":2.8000,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10800121/pdf/","citationCount":"0","resultStr":"{\"title\":\"Progress in the contrary effects of glucagon-like peptide-1 and chemerin on obesity development.\",\"authors\":\"Qilong Zhang, Jianping Ye, Xiaohui Wang\",\"doi\":\"10.1177/15353702231214270\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Glucagon-like peptide-1 (GLP-1), secreted by intestinal L-cells, plays a pivotal role in the modulation of β-cell insulin secretion in a glucose-dependent manner, concurrently promoting β-cell survival and β-cell mass. Notably, GLP-1 has emerged as an effective second-line treatment for type 2 diabetes mellitus, gaining further prominence for its pronounced impact on body weight reduction, positioning it as a potent antiobesity agent. However, the mechanism by which GLP-1 improves obesity remains unclear. Some reports suggest that this mechanism may be associated with the regulation of adipokine synthesis within adipose tissue. Chemerin, a multifunctional adipokine and chemokine, has been identified as a pivotal player in adipocyte differentiation and the propagation of systemic inflammation, a hallmark of obesity. This review provides a comprehensive overview of the mechanisms by which GLP-1 and chemerin play crucial roles in obesity and obesity-related diseases. It discusses well-established aspects, such as their effects on food intake and glycolipid metabolism, as well as recent insights, including their influence on macrophage polarization and adipose tissue thermogenesis. GLP-1 has been shown to increase the population of anti-inflammatory M2 macrophages, promote brown adipose tissue thermogenesis, and induce the browning of white adipose tissue. In contrast, chemerin exhibits opposite effects in these processes. In addition, recent research findings have demonstrated the promising potential of GLP-1-based therapies in directly or indirectly regulating chemerin expression. In an intriguing reciprocal relationship, chemerin has also been newly identified as a negative regulator of GLP-1 <i>in vivo</i>. This review delineates the intricate interplay between GLP-1 and chemerin, unraveling their mutual inhibitory interactions. To the best of our knowledge, no previous reviews have focused on this specific topic, making this review particularly valuable in expanding our understanding of the endocrine mechanisms of obesity and providing potential strategies for the treatment of obesity and related diseases.</p>\",\"PeriodicalId\":12163,\"journal\":{\"name\":\"Experimental Biology and Medicine\",\"volume\":\" \",\"pages\":\"2020-2029\"},\"PeriodicalIF\":2.8000,\"publicationDate\":\"2023-11-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10800121/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Experimental Biology and Medicine\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1177/15353702231214270\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2023/12/6 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q2\",\"JCRName\":\"MEDICINE, RESEARCH & EXPERIMENTAL\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Experimental Biology and Medicine","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1177/15353702231214270","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2023/12/6 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"MEDICINE, RESEARCH & EXPERIMENTAL","Score":null,"Total":0}
引用次数: 0

摘要

胰高血糖素样肽-1 (Glucagon-like peptide-1, GLP-1)由肠道l细胞分泌,以葡萄糖依赖的方式调节β细胞胰岛素分泌,同时促进β细胞存活和β细胞质量。值得注意的是,GLP-1已成为2型糖尿病的有效二线治疗药物,其对体重减轻的显著影响使其成为一种有效的抗肥胖药物。然而,GLP-1改善肥胖的机制尚不清楚。一些报道表明,这一机制可能与脂肪组织内脂肪因子合成的调节有关。趋化素是一种多功能脂肪因子和趋化因子,已被确定为脂肪细胞分化和全身性炎症(肥胖的标志)传播的关键角色。本文综述了GLP-1和趋化素在肥胖和肥胖相关疾病中发挥重要作用的机制。它讨论了成熟的方面,如它们对食物摄入和糖脂代谢的影响,以及最近的见解,包括它们对巨噬细胞极化和脂肪组织产热的影响。GLP-1可增加抗炎M2巨噬细胞数量,促进褐色脂肪组织产热,诱导白色脂肪组织褐化。相反,趋化素在这些过程中表现出相反的作用。此外,最近的研究结果表明,基于glp -1的治疗在直接或间接调节趋化素表达方面具有很大的潜力。在一个有趣的互惠关系中,chemerin也被新发现是体内GLP-1的负调节因子。这篇综述描述了GLP-1和趋化素之间复杂的相互作用,揭示了它们相互抑制的相互作用。据我们所知,之前还没有针对这一特定主题的综述,这使得本综述在扩大我们对肥胖内分泌机制的理解以及为肥胖及相关疾病的治疗提供潜在策略方面特别有价值。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
Progress in the contrary effects of glucagon-like peptide-1 and chemerin on obesity development.

Glucagon-like peptide-1 (GLP-1), secreted by intestinal L-cells, plays a pivotal role in the modulation of β-cell insulin secretion in a glucose-dependent manner, concurrently promoting β-cell survival and β-cell mass. Notably, GLP-1 has emerged as an effective second-line treatment for type 2 diabetes mellitus, gaining further prominence for its pronounced impact on body weight reduction, positioning it as a potent antiobesity agent. However, the mechanism by which GLP-1 improves obesity remains unclear. Some reports suggest that this mechanism may be associated with the regulation of adipokine synthesis within adipose tissue. Chemerin, a multifunctional adipokine and chemokine, has been identified as a pivotal player in adipocyte differentiation and the propagation of systemic inflammation, a hallmark of obesity. This review provides a comprehensive overview of the mechanisms by which GLP-1 and chemerin play crucial roles in obesity and obesity-related diseases. It discusses well-established aspects, such as their effects on food intake and glycolipid metabolism, as well as recent insights, including their influence on macrophage polarization and adipose tissue thermogenesis. GLP-1 has been shown to increase the population of anti-inflammatory M2 macrophages, promote brown adipose tissue thermogenesis, and induce the browning of white adipose tissue. In contrast, chemerin exhibits opposite effects in these processes. In addition, recent research findings have demonstrated the promising potential of GLP-1-based therapies in directly or indirectly regulating chemerin expression. In an intriguing reciprocal relationship, chemerin has also been newly identified as a negative regulator of GLP-1 in vivo. This review delineates the intricate interplay between GLP-1 and chemerin, unraveling their mutual inhibitory interactions. To the best of our knowledge, no previous reviews have focused on this specific topic, making this review particularly valuable in expanding our understanding of the endocrine mechanisms of obesity and providing potential strategies for the treatment of obesity and related diseases.

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
Experimental Biology and Medicine
Experimental Biology and Medicine 医学-医学:研究与实验
CiteScore
6.00
自引率
0.00%
发文量
157
审稿时长
1 months
期刊介绍: Experimental Biology and Medicine (EBM) is a global, peer-reviewed journal dedicated to the publication of multidisciplinary and interdisciplinary research in the biomedical sciences. EBM provides both research and review articles as well as meeting symposia and brief communications. Articles in EBM represent cutting edge research at the overlapping junctions of the biological, physical and engineering sciences that impact upon the health and welfare of the world''s population. Topics covered in EBM include: Anatomy/Pathology; Biochemistry and Molecular Biology; Bioimaging; Biomedical Engineering; Bionanoscience; Cell and Developmental Biology; Endocrinology and Nutrition; Environmental Health/Biomarkers/Precision Medicine; Genomics, Proteomics, and Bioinformatics; Immunology/Microbiology/Virology; Mechanisms of Aging; Neuroscience; Pharmacology and Toxicology; Physiology; Stem Cell Biology; Structural Biology; Systems Biology and Microphysiological Systems; and Translational Research.
期刊最新文献
STEMIN and YAP5SA, the future of heart repair? Fructose metabolism is unregulated in cancers and placentae. Subunit-specific mechanisms of isoflurane-induced acute tonic inhibition in dentate gyrus granule neuron. Quantitative characterization of retinal features in translated OCTA. Exosomal circPTPRK promotes angiogenesis after radiofrequency ablation in hepatocellular carcinoma.
×
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
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 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 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1