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慢性胰腺炎继发胰岛素依赖型糖尿病患者的代谢控制与B细胞功能

Metabolic control and B cell function in patients with insulin-dependent diabetes mellitus secondary to chronic pancreatitis.

作者信息

Larsen S, Hilsted J, Tronier B, Worning H

机构信息

Medical Department F, Glostrup Hospital, Denmark.

出版信息

Metabolism. 1987 Oct;36(10):964-7. doi: 10.1016/0026-0495(87)90133-8.

Abstract

Among 88 unselected patients with chronic pancreatitis 35% (95% confidence limits 25 to 46) had insulin-dependent diabetes, 31% (21% to 41%) had non-insulin-dependent diabetes or impaired glucose tolerance (by intravenous glucose tolerance test), and 34% (24% to 45%) had normal glucose tolerance. B cell function measured by C-peptide concentration after 1 mg glucagon IV correlated with the pancreatic enzyme secretion (meal stimulated duodenal lipase content). B cell function was preserved to a greater extent (P less than .01), and glycosylated hemoglobin and fasting level of glucose were lower (P less than .01 to .05) in the 31 patients with pancreatogenic diabetes than than in 35 otherwise comparable patients with type I (insulin-dependent) diabetes, yet daily insulin dose was similar in the two groups. Glucagon stimulated C-peptide was inversely correlated to glycosylated hemoglobin in insulin-dependent patients with pancreatogenic diabetes and in type I diabetes. Since body mass indices were identical in the two groups, better glucoregulation was not due to reduced food intake or malabsorption in pancreatogenic diabetes. Rather residual B cell function and/or different secretion of other pancreatic hormones in pancreatogenic diabetes may account for different metabolic control in type I IDDM compared with insulin-dependent pancreatogenic diabetes.

摘要

在88例未经挑选的慢性胰腺炎患者中,35%(95%置信区间为25%至46%)患有胰岛素依赖型糖尿病,31%(21%至41%)患有非胰岛素依赖型糖尿病或糖耐量受损(通过静脉葡萄糖耐量试验测定),34%(24%至45%)糖耐量正常。静脉注射1毫克胰高血糖素后通过C肽浓度测定的B细胞功能与胰腺酶分泌(进食刺激后的十二指肠脂肪酶含量)相关。与35例其他情况相当的I型(胰岛素依赖型)糖尿病患者相比,31例胰腺性糖尿病患者的B细胞功能保留程度更高(P<0.01),糖化血红蛋白和空腹血糖水平更低(P<0.01至0.05),但两组的每日胰岛素剂量相似。在胰岛素依赖型胰腺性糖尿病患者和I型糖尿病患者中,胰高血糖素刺激后的C肽与糖化血红蛋白呈负相关。由于两组的体重指数相同,胰腺性糖尿病患者更好的血糖调节并非由于食物摄入量减少或吸收不良。相反,胰腺性糖尿病中残余的B细胞功能和/或其他胰腺激素的不同分泌可能是导致I型胰岛素依赖型糖尿病(IDDM)与胰岛素依赖型胰腺性糖尿病代谢控制不同的原因。

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