{"title":"[Glucose intolerance in injured patients (author's transl)].","authors":"P Bouletreau, Y Page, J Motin","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>Glucose intolerance occurring in injured patients is known to be a part of the general response to injury described by Cuthbbertson: early \"ebb phase\" with a decrease of energy production, then \"flow phase\" with hypermetabolism. Several processes can be responsible for the abnormalities observed: 1) Alterations in peripheral glucose uptake. 2) Absolute or relative insulin lack in connection with increased catecholamine release which is know to inhibit insulin secretion. 3) Decreased sensitivity and responsiveness to insulin in connection with increased levels of counter regulatory hormones (catecholamines, glucagon, growth hormone). 4) Non-suppressibility of hepatic gluconeogenesis by glucose. Glucose intolerance decreases glucose utilisation and leads to increased proteolysis always unfavorable for patients.</p>","PeriodicalId":7785,"journal":{"name":"Anesthesie, analgesie, reanimation","volume":"38 3-4","pages":"95-100"},"PeriodicalIF":0.0000,"publicationDate":"1981-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Anesthesie, analgesie, reanimation","FirstCategoryId":"1085","ListUrlMain":"","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
Glucose intolerance occurring in injured patients is known to be a part of the general response to injury described by Cuthbbertson: early "ebb phase" with a decrease of energy production, then "flow phase" with hypermetabolism. Several processes can be responsible for the abnormalities observed: 1) Alterations in peripheral glucose uptake. 2) Absolute or relative insulin lack in connection with increased catecholamine release which is know to inhibit insulin secretion. 3) Decreased sensitivity and responsiveness to insulin in connection with increased levels of counter regulatory hormones (catecholamines, glucagon, growth hormone). 4) Non-suppressibility of hepatic gluconeogenesis by glucose. Glucose intolerance decreases glucose utilisation and leads to increased proteolysis always unfavorable for patients.