Pancreatic Islets in Mice with the Obese-hyperglycemic Syndrome: Lack of Effect of Carbutamide
Pancreatic Islets in Mice with the Obese-hyperglycemic Syndrome: Lack of Effect of Carbutamide
复制标题
肥胖高血糖综合征小鼠的胰岛：卡丁酰胺缺乏作用
作者：
W. Gepts;Brussels Jean Christophe;J. Mayer
遗传性肥胖高血糖综合征是一种孟德尔隐性遗传疾病，近年来得到了深入研究。特别是，患有这种综合征的小鼠严重肥胖（已记录体重高达 115 克）、高胆固醇血症、高血糖水平通常因生长激素的施用而进一步增加、即使禁食时脂肪生成也会增加、糖原周转增加、肝脏磷酸化酶增加*以及许多其他营养、内分泌和行为特质。从病因学的角度来看，特别令人感兴趣的事实是，朗格汉斯胰岛严重肥大，胰腺的胰岛素含量增加，其血清的胰岛素样活性高于非肥胖动物，门田和绿川发现二乙基二硫代氨基甲酸盐具有α细胞毒性，可降低血糖并消除对生长激素的高血糖反应，并且生长后胰腺胰高血糖素含量似乎增加还发现卡丁酰胺不能纠正这些动物中碳水化合物代谢和脂肪代谢的缺陷。
The hereditary obese-hyperglycemic syndrome is a Mendelian recessive condition which has been intensively studied in the last few years. In particular, mice with this syndrome are grossly obese (weights up to 115 gm. have been recorded), hypercholesterolemic, show high blood glucose levels generally further increased by the administration of growth hormone, an increased lipogenesis even when fasted, increased glycogen turnover, increased liver phosphorylase,* and a number of other nutritional, endocrine and behavioral idiosyncrasies. Of particular interest from the etiological point of view is the fact that the islets of Langerhans are grossly hypertrophied," that the insulin content of the pancreas is increased, that the insulin-like activity of their serum is greater than that of the nonobese animals, that diethyldithiocarbamate, which Kadota and Midorikawa found to be alphacytotoxic, decreases blood sugar and eliminates the hyperglycemic reaction to growth hormone and that the pancreatic glucagon content appears increased after growth hormone administration. It has also been found that carbutamide did not correct the defects in carbohydrate metabolism and in fat metabolism found in these animals.