帅怡, 王彦琴, 董妙珠, 马国云, 叶文锐, 王俐, 蔡美琴, 肖萍, 仲伟鉴. 蔗糖喂饲GK大鼠和Wistar大鼠致胰腺病理结构的改变[J]. 环境与职业医学, 2010, 27(11): 657-659,663.
引用本文: 帅怡, 王彦琴, 董妙珠, 马国云, 叶文锐, 王俐, 蔡美琴, 肖萍, 仲伟鉴. 蔗糖喂饲GK大鼠和Wistar大鼠致胰腺病理结构的改变[J]. 环境与职业医学, 2010, 27(11): 657-659,663.
SHUAI Yi , WANG Yan-qin , DONG Miao-zhu , MA Guo-yun , YE Wen-rui , WANG Li , CAI Mei-qin , XIAO Ping , ZHONG Wei-jian . Effect of Sucrose on Pathological Change of Pancreas in GK and Wistar Rats[J]. Journal of Environmental and Occupational Medicine, 2010, 27(11): 657-659,663.
Citation: SHUAI Yi , WANG Yan-qin , DONG Miao-zhu , MA Guo-yun , YE Wen-rui , WANG Li , CAI Mei-qin , XIAO Ping , ZHONG Wei-jian . Effect of Sucrose on Pathological Change of Pancreas in GK and Wistar Rats[J]. Journal of Environmental and Occupational Medicine, 2010, 27(11): 657-659,663.

蔗糖喂饲GK大鼠和Wistar大鼠致胰腺病理结构的改变

Effect of Sucrose on Pathological Change of Pancreas in GK and Wistar Rats

  • 摘要: 目的 观察蔗糖喂饲Goto-Kakizak (i 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。

     

    Abstract: Objective To observe the effect of sucrose on pathological and ultrastructural change of pancreas in GotoKakizaki (GK)and Wistar rats.

    Methods GK (n=26) and Wistar rats (n=26)were randomly divided into four groups:Wistar(W)group, Wistar+30% sucrose(WS)group, GK(G)group, GK+30% sucrose(GS)group. WS and GS group were fed with 30% sucrose water, while W and G group with plain water. All animals were sacrificed after 6 weeks. The pathological changes of pancreas were observed using histochemical staining and electro-microscope.

    Results After fed with 30% sucrose water, fibrosis of islets was seen and the number of pancreatic β-cell decreased significantly in WS group. Furthermore, irregular deform of nucleus, significant reduction of the secretary granules within cells, and vacuolization of mitochondria was demonstrated in WS group. Compared with WS group, more serious fibrosis of islets was observed and pancreatic β-cells were only sporadically visible in GS group; in addition, kayro-pyknosis, substantial reduction of the secretary granules in cells, severe vacuolization of mitochondria, ridge dissolution and fracture, and severe pancreatic pathological changes were also observed in GS group.

    Conclusion High sucrose intake could induce and aggravate pancreatic pathological lesions in GK and Wistar rats, suggesting that GK rats fed with 30% sucrose water could be used as an animal model for non-obese diabetes study.

     

/

返回文章
返回