Regional melatonin and somatostatin dependent mechanisms in pancreatic incretory activity and in intestinal bacterial homeostasis.

A. Muradyan
{"title":"Regional melatonin and somatostatin dependent mechanisms in pancreatic incretory activity and in intestinal bacterial homeostasis.","authors":"A. Muradyan","doi":"10.56936/18290825-2022.16.4-6","DOIUrl":null,"url":null,"abstract":"For many years, it was generally accepted that melatonin and somatostatin have intracerebral sources of synthesis.\nMelatonin is produced in the pineal gland and somatostatin in the hypothalamus. However, there are very informative data regarding the extracerebral sources of melatonin and somatostatin synthesis in numerous literary sources published over the past 60 years. At the same time, the biological purpose of extracerebral somatostatin and melatonin has been insufficiently studied. This article presents the readers with an analysis of modern literature and the results of own researches on the biological role of melatonin and somatostatin produced in the pancreas and intestinal tract.\nUnder experimental conditions on arginine-induced acute pancreatitis model in rats, structural and hormonal changes were studied in the pancreas, mucosa of the small and large intestines in regional pathological process using morphological, morphometric, immunomorphological and enzyme immunoassay methods.\nAccording to the morphological and morphometric analysis results, gross dystrophic changes in the pancreas and intestinal mucosa were observed at relatively early stages of the pathological process – in 2 and 24 hours after the arginine administration. Immunomorphological studies established that the content of melatonin-positive secretory cells noticeably decreased, especially in the areas of mucosal damage in this very period of the pathological process in pancreas, in the mucous membrane of the small and large intestines. At the same time, the content of somatotropin in blood serum and pancreas markedly increased during the indicated period of the experiment.\nSevere dystrophic processes on small intestinal mucosa, which are particularly expressed by inhibition of local melatonin-secreting cell function, apparently exclude the inhibitory effect of melatonin on somatostatin synthesis process in pancreas. It is not excluded that there is a directed activation of pancreatic delta cells responsible for the somatostatin synthesis at relatively early stages of “arginine pancreatitis”.\nBased on our own researches in context with available very informative literature data, we can conclude that extrapineal melatonin and extrahypothalamic somatostatin should be given an important role in the integrative activity of organ-digestive system – the pancreas and small intestine.","PeriodicalId":353660,"journal":{"name":"THE NEW ARMENIAN MEDICAL JOURNAL","volume":"4 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"1900-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"THE NEW ARMENIAN MEDICAL JOURNAL","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.56936/18290825-2022.16.4-6","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

For many years, it was generally accepted that melatonin and somatostatin have intracerebral sources of synthesis. Melatonin is produced in the pineal gland and somatostatin in the hypothalamus. However, there are very informative data regarding the extracerebral sources of melatonin and somatostatin synthesis in numerous literary sources published over the past 60 years. At the same time, the biological purpose of extracerebral somatostatin and melatonin has been insufficiently studied. This article presents the readers with an analysis of modern literature and the results of own researches on the biological role of melatonin and somatostatin produced in the pancreas and intestinal tract. Under experimental conditions on arginine-induced acute pancreatitis model in rats, structural and hormonal changes were studied in the pancreas, mucosa of the small and large intestines in regional pathological process using morphological, morphometric, immunomorphological and enzyme immunoassay methods. According to the morphological and morphometric analysis results, gross dystrophic changes in the pancreas and intestinal mucosa were observed at relatively early stages of the pathological process – in 2 and 24 hours after the arginine administration. Immunomorphological studies established that the content of melatonin-positive secretory cells noticeably decreased, especially in the areas of mucosal damage in this very period of the pathological process in pancreas, in the mucous membrane of the small and large intestines. At the same time, the content of somatotropin in blood serum and pancreas markedly increased during the indicated period of the experiment. Severe dystrophic processes on small intestinal mucosa, which are particularly expressed by inhibition of local melatonin-secreting cell function, apparently exclude the inhibitory effect of melatonin on somatostatin synthesis process in pancreas. It is not excluded that there is a directed activation of pancreatic delta cells responsible for the somatostatin synthesis at relatively early stages of “arginine pancreatitis”. Based on our own researches in context with available very informative literature data, we can conclude that extrapineal melatonin and extrahypothalamic somatostatin should be given an important role in the integrative activity of organ-digestive system – the pancreas and small intestine.
区域褪黑素和生长抑素在胰腺分泌活性和肠道细菌稳态中的依赖机制。
多年来,人们普遍认为褪黑素和生长抑素是脑内合成的。褪黑素在松果体中产生,生长抑素在下丘脑中产生。然而,在过去60年出版的大量文献中,关于褪黑素和生长抑素合成的脑外来源有非常翔实的数据。同时,对脑外生长抑素和褪黑素的生物学作用研究不足。这篇文章向读者介绍了对褪黑激素和生长抑素在胰腺和肠道中产生的生物学作用的现代文献分析和自己的研究结果。在精氨酸诱导的大鼠急性胰腺炎模型的实验条件下,采用形态学、形态计量学、免疫形态学和酶免疫分析法研究了胰腺、小肠和大肠黏膜在局部病理过程中的结构和激素变化。根据形态学和形态计量学分析结果,在病理过程的较早阶段-精氨酸给药后2和24小时,胰腺和肠粘膜出现了明显的营养不良变化。免疫形态学研究证实,褪黑激素阳性分泌细胞的含量明显减少,特别是在病理过程的这一时期胰腺粘膜损伤区域,小肠和大肠粘膜。同时,血清和胰腺中促生长激素含量在实验指定期间显著升高。小肠黏膜的严重营养不良过程,特别是通过抑制局部褪黑素分泌细胞功能来表达,显然排除了褪黑素对胰腺生长抑素合成过程的抑制作用。不排除在“精氨酸性胰腺炎”的相对早期阶段,负责生长抑素合成的胰三角洲细胞有定向激活。根据我们自己的研究和现有的非常丰富的文献数据,我们可以得出结论,肾上腺外褪黑素和下丘脑外生长抑素应该在器官消化系统-胰腺和小肠的整合活动中发挥重要作用。
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
自引率
0.00%
发文量
0
×
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