Role of Glucagon in The Metabolic Response

Azwar Iwan Tona, Maimun Syukri
{"title":"Role of Glucagon in The Metabolic Response","authors":"Azwar Iwan Tona, Maimun Syukri","doi":"10.47353/jsocmed.v2i2.62","DOIUrl":null,"url":null,"abstract":"Historically, glucagon is the counter-regulatory hormone of insulin. Glucagon secretion is induced by fasting conditions or hypoglycaemia to increase glucose levels. Glucagon is the dominant product of alpha cells in the islet and was first identified in 1923 during an attempt to purify insulin, where it was identified as a contaminant hyperglycaemia factor. Further research determined that the hyperglycaemic action of glucagon is mediated by increased hepatic glycogenolysis and gluconeogenesis to increase endogenous glucose production. Insulin and glucagon as opposing hormones work together for glycaemic control. Diabetic hyperglycaemia is caused by increased impaired insulin action and inappropriately elevated glucagon levels. This review summarizes an important function of glucagon is its role as a regulator of glucose homeostasis. Increased plasma glucagon levels lead to increased hepatic glucose production. The balance between insulin and glucagon is responsible for maintaining euglycaemia conditions. In conditions of hypoglycaemia, increased glucagon secretion leads to increased hepatic glucose production through a number of cellular mechanisms including suppression of glycogenesis and glycolysis and stimulation of glycogenolysis and gluconeogenesis","PeriodicalId":496210,"journal":{"name":"Journal of Society Medicine","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2023-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Society Medicine","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.47353/jsocmed.v2i2.62","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

Historically, glucagon is the counter-regulatory hormone of insulin. Glucagon secretion is induced by fasting conditions or hypoglycaemia to increase glucose levels. Glucagon is the dominant product of alpha cells in the islet and was first identified in 1923 during an attempt to purify insulin, where it was identified as a contaminant hyperglycaemia factor. Further research determined that the hyperglycaemic action of glucagon is mediated by increased hepatic glycogenolysis and gluconeogenesis to increase endogenous glucose production. Insulin and glucagon as opposing hormones work together for glycaemic control. Diabetic hyperglycaemia is caused by increased impaired insulin action and inappropriately elevated glucagon levels. This review summarizes an important function of glucagon is its role as a regulator of glucose homeostasis. Increased plasma glucagon levels lead to increased hepatic glucose production. The balance between insulin and glucagon is responsible for maintaining euglycaemia conditions. In conditions of hypoglycaemia, increased glucagon secretion leads to increased hepatic glucose production through a number of cellular mechanisms including suppression of glycogenesis and glycolysis and stimulation of glycogenolysis and gluconeogenesis
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
胰高血糖素在代谢反应中的作用
从历史上看,胰高血糖素是胰岛素的反调节激素。胰高血糖素的分泌是由空腹或低血糖引起的,以增加血糖水平。胰高血糖素是胰岛α细胞的主要产物,1923年在试图纯化胰岛素时首次被发现,当时它被确定为一种污染性高血糖因子。进一步的研究确定胰高血糖素的高血糖作用是通过增加肝糖原溶解和糖异生来增加内源性葡萄糖的产生。胰岛素和胰高血糖素作为对立激素共同控制血糖。糖尿病性高血糖是由胰岛素作用受损和胰高血糖素水平不适当升高引起的。本文综述了胰高血糖素的一项重要功能,即调节葡萄糖稳态。血浆胰高血糖素水平升高导致肝糖生成增加。胰岛素和胰高血糖素之间的平衡负责维持血糖状况。在低血糖的情况下,胰高血糖素分泌的增加通过多种细胞机制导致肝脏葡萄糖产量增加,包括抑制糖原分解和糖酵解,刺激糖原分解和糖异生
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 去求助
来源期刊
自引率
0.00%
发文量
0
期刊最新文献
Role of Glucagon in The Metabolic Response
×
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