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糖尿病啮齿动物小肠肌肉的结构和功能特征

Structural and functional characteristics of muscle from diabetic rodent small intestine.

作者信息

Nowak T V, Harrington B, Weisbruch J P, Kalbfleisch J H

机构信息

Department of Medicine, Medical College of Wisconsin, Milwaukee 53225.

出版信息

Am J Physiol. 1990 May;258(5 Pt 1):G690-8. doi: 10.1152/ajpgi.1990.258.5.G690.

DOI:10.1152/ajpgi.1990.258.5.G690
PMID:2185667
Abstract

After 30 days of streptozotocin-induced diabetes, the small intestine from untreated diabetic, insulin-treated diabetic, and nondiabetic rodents was excised in toto and measured. Despite a net loss in body weight, the diabetic animals showed a near twofold increase in small intestinal weight. This was characterized by a 148% increase in mucosal mass as well as a 39% increase in intestinal smooth muscle mass (P less than 0.05, respectively). The diabetic intestine was significantly longer and had a greater diameter and surface area. Diabetes significantly increased mucosal mass per unit surface area but produced an insignificant decrease in smooth muscle mass per unit surface area. Insulin treatment of the diabetic animals prevented the increase in total mucosal mass and mucosal mass per unit surface area. Insulin treatment also prevented the increase in smooth muscle mass, but reduced smooth muscle mass per unit surface area to a level significantly less than that found in nondiabetic intestine. In vitro dose-response studies of circular and longitudinal small intestinal muscle from the diabetic animals showed normal tension development and sensitivity to both bethanechol chloride and physostigmine. These observations show that the diabetic state produces alterations in not only mucosal but also smooth muscle mass in the small intestine. However, despite these morphological changes, diabetic intestinal smooth muscle retains its sensitivity to cholinergic stimulation and its capacity for tension generation.

摘要

在链脲佐菌素诱导糖尿病30天后,将未治疗的糖尿病、胰岛素治疗的糖尿病和非糖尿病啮齿动物的小肠完整切除并进行测量。尽管体重出现净损失,但糖尿病动物的小肠重量增加了近两倍。其特征为黏膜质量增加148%以及肠平滑肌质量增加39%(P均小于0.05)。糖尿病小肠明显更长,直径和表面积更大。糖尿病显著增加了单位表面积的黏膜质量,但单位表面积的平滑肌质量出现不显著的减少。对糖尿病动物进行胰岛素治疗可防止总黏膜质量和单位表面积黏膜质量增加。胰岛素治疗还可防止平滑肌质量增加,但使单位表面积的平滑肌质量降至显著低于非糖尿病小肠的水平。对糖尿病动物的小肠环形肌和纵行肌进行体外剂量反应研究显示,其张力发展正常,对氯化贝胆碱和毒扁豆碱均敏感。这些观察结果表明,糖尿病状态不仅会导致小肠黏膜质量改变,还会引起平滑肌质量改变。然而,尽管存在这些形态学变化,糖尿病肠平滑肌仍保留对胆碱能刺激的敏感性及其产生张力的能力。

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