{"title":"Pancreatic islet hypertrophy in spontaneous maturity onset obese-diabetic CBA/Ca mice","authors":"Carlos D. Figueroa , Peter V. Taberner","doi":"10.1016/0020-711X(94)90099-X","DOIUrl":null,"url":null,"abstract":"<div><p>Mature male CBA/Ca mice develop a spontaneous mild diabetes-obesity syndrome which is characterized by hyperglycaemia, hyperinsulinaemia and insulin resistance, and resembles human Type II diabetes mellitus. Immunocytochemical staining of pancreas sections for insulin showed that the pancreas from mature obese mice possessed significantly enlarged islets compared to those from age-matched control (lean) mice. The pancreatic insulin content was significantly greater in 24-week-old obese mice (1.78 ± 0.14mU/mg) compared with lean controls (0.92 ± 0.09 mU/mg). This increase was still apparent at 48 weeks of age. We conclude that, unlike most other rodent models of Type II diabetes, there is no chronic degeneration of beta cells in these mice, so that circulating insulin levels remain high throughout their life. We suggest, therefore, that the male CBA/Ca mouse represents a valuable model for investigating maturity onset diabetes.</p></div>","PeriodicalId":13733,"journal":{"name":"International Journal of Biochemistry","volume":"26 10","pages":"Pages 1299-1303"},"PeriodicalIF":0.0000,"publicationDate":"1994-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0020-711X(94)90099-X","citationCount":"16","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"International Journal of Biochemistry","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/0020711X9490099X","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 16
Abstract
Mature male CBA/Ca mice develop a spontaneous mild diabetes-obesity syndrome which is characterized by hyperglycaemia, hyperinsulinaemia and insulin resistance, and resembles human Type II diabetes mellitus. Immunocytochemical staining of pancreas sections for insulin showed that the pancreas from mature obese mice possessed significantly enlarged islets compared to those from age-matched control (lean) mice. The pancreatic insulin content was significantly greater in 24-week-old obese mice (1.78 ± 0.14mU/mg) compared with lean controls (0.92 ± 0.09 mU/mg). This increase was still apparent at 48 weeks of age. We conclude that, unlike most other rodent models of Type II diabetes, there is no chronic degeneration of beta cells in these mice, so that circulating insulin levels remain high throughout their life. We suggest, therefore, that the male CBA/Ca mouse represents a valuable model for investigating maturity onset diabetes.