{"title":"[Anomalies of insulin secretion and type 2 diabetes: recent information].","authors":"P J Guillausseau","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>Beta-cell dysfunction is prominent in Type 2 (non-insulin-dependent) diabetes mellitus. Four types of abnormalities have been described. Oscillatory pattern of insulin-secretion is impaired, with a loss of high frequency pulses and with a reduction in amplitude of slow oscillations. This impairment takes place early in the course of the disease, as does the loss of the first phase of insulin secretion after intravenous glucose. Quantitative (insulin deficiency in relative and absolute terms) and qualitative abnormalities (excess in proinsulin and in 32-33 split proinsulin) have been also observed in Type 2 diabetes. One or several genetic defects seem to be responsible for the development of this beta-cell dysfunction and for Type 2 diabetes mellitus.</p>","PeriodicalId":11111,"journal":{"name":"Diabete & metabolisme","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"1994-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Diabete & metabolisme","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
Beta-cell dysfunction is prominent in Type 2 (non-insulin-dependent) diabetes mellitus. Four types of abnormalities have been described. Oscillatory pattern of insulin-secretion is impaired, with a loss of high frequency pulses and with a reduction in amplitude of slow oscillations. This impairment takes place early in the course of the disease, as does the loss of the first phase of insulin secretion after intravenous glucose. Quantitative (insulin deficiency in relative and absolute terms) and qualitative abnormalities (excess in proinsulin and in 32-33 split proinsulin) have been also observed in Type 2 diabetes. One or several genetic defects seem to be responsible for the development of this beta-cell dysfunction and for Type 2 diabetes mellitus.