Increased muscle glucose uptake during contractions: no need for insulin.

E. Richter, T. Ploug, H. Galbo
{"title":"Increased muscle glucose uptake during contractions: no need for insulin.","authors":"E. Richter, T. Ploug, H. Galbo","doi":"10.1249/00005768-198404000-00313","DOIUrl":null,"url":null,"abstract":"We reinvestigated the prevailing concept that muscle contractions only elicit increased muscle glucose uptake in the presence of a so-called \"permissive\" concentration of insulin (Berger et al., Biochem. J. 146: 231-238, 1975; Vranic and Berger, Diabetes 28: 147-163, 1979). Hindquarters from rats in severe ketoacidosis were perfused with a perfusate containing insulin antiserum. After 60 min perfusion, electrical stimulation increased glucose uptake of the contracting muscles fivefold. Also, subsequent contractions increased glucose uptake in hindquarters from nondiabetic rats perfused for 1.5 h in the presence of antiserum. 3-O-methylglucose uptake was increased markedly by contractions in fast-twitch red and white fibers that were severely glycogen depleted but not in slow-twitch red fibers that were not glycogen depleted. In hindquarters from ketoacidotic rats perfused exactly as by Berger et al., 3-O-methylglucose uptake increased during contractions and glucose uptake was negative at rest and zero during contractions. An increase in muscle transport and uptake of glucose during contractions does not require the presence of insulin. Furthermore, glucose transport in contracting muscle may only increase if glycogen is depleted.","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"96 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"1984-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"214","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"The American journal of physiology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1249/00005768-198404000-00313","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 214

Abstract

We reinvestigated the prevailing concept that muscle contractions only elicit increased muscle glucose uptake in the presence of a so-called "permissive" concentration of insulin (Berger et al., Biochem. J. 146: 231-238, 1975; Vranic and Berger, Diabetes 28: 147-163, 1979). Hindquarters from rats in severe ketoacidosis were perfused with a perfusate containing insulin antiserum. After 60 min perfusion, electrical stimulation increased glucose uptake of the contracting muscles fivefold. Also, subsequent contractions increased glucose uptake in hindquarters from nondiabetic rats perfused for 1.5 h in the presence of antiserum. 3-O-methylglucose uptake was increased markedly by contractions in fast-twitch red and white fibers that were severely glycogen depleted but not in slow-twitch red fibers that were not glycogen depleted. In hindquarters from ketoacidotic rats perfused exactly as by Berger et al., 3-O-methylglucose uptake increased during contractions and glucose uptake was negative at rest and zero during contractions. An increase in muscle transport and uptake of glucose during contractions does not require the presence of insulin. Furthermore, glucose transport in contracting muscle may only increase if glycogen is depleted.
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
收缩时肌肉葡萄糖摄取增加:不需要胰岛素。
我们重新研究了流行的概念,即肌肉收缩只会在所谓的“允许”胰岛素浓度存在时引起肌肉葡萄糖摄取增加(Berger等人,Biochem)。[j] . 21 (2);Vranic和Berger,糖尿病28:147-163,1979)。用含胰岛素抗血清的灌注液灌注严重酮症酸中毒大鼠后腿。灌注60分钟后,电刺激使收缩肌肉的葡萄糖摄取增加了5倍。此外,随后的收缩增加了非糖尿病大鼠在抗血清存在下灌注1.5小时后后腿的葡萄糖摄取。3- o -甲基葡萄糖摄取在糖原严重耗尽的快速收缩红纤维和白纤维中显著增加,而在糖原未耗尽的慢收缩红纤维中则没有明显增加。在与Berger等人完全相同灌注的酮症酸中毒大鼠的后腿中,3- o -甲基葡萄糖摄取在收缩期间增加,葡萄糖摄取在静止时为负,在收缩期间为零。收缩时肌肉运输和葡萄糖摄取的增加不需要胰岛素的存在。此外,只有当糖原耗尽时,收缩肌肉中的葡萄糖转运才会增加。
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
Now what? Protein kinase A phosphorylation is involved in regulated exocytosis of aquaporin-2 in transfected LLC-PK1 cells. Hepatocytes in the bile duct-ligated rat express Bcl-2. Synergistic vascular effects of dietary sodium supplementation and angiotensin II administration. Recombinant thrombomodulin prevents endotoxin-induced lung injury in rats by inhibiting leukocyte activation.
×
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