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[目的]观察蔗糖喂饲Goto-Kakizaki(GK)大鼠和Wistar大鼠致胰腺病理结构及超微结构的改变。[方法][GK和Wistar大鼠各26只,随机分为(1)Wistar(W)组;(2)Wistar+30%蔗糖(WS)组;(3)GK(G)组;(4)GK+30%蔗糖(GS)组。WS、GS组给予30%蔗糖饮水,另两组给予正常饮水。实验第6周结束时处死动物,分离胰腺,采用组织化学染色法及电镜技术对其组织结构改变进行观察。[结果]给予30%蔗糖饮水后,Wistar大鼠胰岛出现一定程度的纤维化,胰岛β细胞数量显著下降,细胞核出现不规则变形,细胞内分泌颗粒明显减少,线粒体出现空泡变性;与Wistar大鼠相比,GK大鼠给予30%蔗糖饮水后胰岛组织出现严重的纤维化病变,胰岛β细胞仅零星可见,细胞核出现固缩,细胞内分泌颗粒大量减少,线粒体严重空泡变,并出现嵴溶解和嵴断裂,胰岛组织出现更为严重的病理改变。[结论]高蔗糖摄入可引起或加重GK和Wistar大鼠胰腺的病理性损伤,提示30%蔗糖喂饲GK大鼠可以用作非肥胖型糖尿病胰腺病变动物模型的优先品种。
[Objective] To observe the pathological and ultrastructural changes of pancreatic tissue in sucrose fed Goto-Kakizaki (GK) rats and Wistar rats. [Methods] Twenty-six GK and Wistar rats were randomly divided into (1) Wistar (W) group, (2) Wistar + 30% sucrose group, (3) GK GK + 30% sucrose (GS) group. WS, GS group given 30% sucrose drinking water, the other two groups given normal drinking water. At the end of the sixth week, the animals were sacrificed and the pancreas was isolated. The histological changes were observed by histochemical staining and electron microscopy. [Result] After 30% sucrose drinking water, there was a certain degree of fibrosis in islet of Wistar rats, the number of islet β cells was significantly decreased, the nucleus was irregularly deformed, the endocrine granules were obviously reduced and the mitochondria were vacuolar degeneration. Compared with Wistar rats In contrast, GK rats were given 30% sucrose drinking water after islet fibrosis, pancreatic islet β cells only sporadic, nuclear shrinkage, a significant reduction in the number of endocrine cells, mitochondria severe vacuolar change, and the emergence of crest lysis and Crista fracture, islet tissue more serious pathological changes. [Conclusion] High sucrose intake can cause or aggravate the pathological injury of pancreas in GK and Wistar rats, suggesting that 30% sucrose fed GK rats can be used as the priority species in the animal model of non-obese diabetic pancreas lesions.