{"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.
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。