Previous results from our laboratory showed that chitosan biguanidine hydrochloride (CSGH) and chitooligosaccharide guanidine (COSG) could control glucose uptake by regulating the expression of glucose transporters (GLUTs) in vitro experiments. In this study, we try to delineate changes observed in activation of diacylglycerol (DAG)/protein kinase C-β(PKC-β) pathway and GLUT2 in kidney. STZ-induced diabetic rats were administered COSG via daily intra-gastric gavage for 8 weeks. Obviously, COSG significantly attenuated fasting blood glucose and blood glucose level by modulating the over-expression of GLUT2 and the level of DAG as well. Immunohistological examination revealed that factors such as PKC-β and transforming growth factor-β (TGF-β) diminished to various extents after treatment with COSG, which impinged on the synthesis of extracellular matrix (ECM) components like fibronectin (FN). As a result, high glucose-induced activation of DAG/PKC pathway is inhibited, which is associated with the concentration of glucose controlled by the expression of GLUT2 with the treatment of COSG.

我们实验室的先前结果表明，壳聚糖双胍盐酸盐（CSGH）和壳寡糖胍（COSG）可以通过调节体外实验中葡萄糖转运蛋白（GLUTs）的表达来控制葡萄糖的摄取。在这项研究中，我们试图描绘甘油二酯的活化（DAG）观察到变化/蛋白激酶C- β（PKC- β）途径和GLUT2肾。每天通过胃内管饲法对STZ诱导的糖尿病大鼠进行COSG，持续8周。显然，COSG通过调节GLUT2的过表达和DAG的水平显着降低了空腹血糖和血糖水平。免疫组织学检查发现的因素，如PKC- β和转化生长因子β用COSG处理后，TGF- β（TGF- β）有不同程度的降低，这影响了诸如纤连蛋白（FN）之类的细胞外基质（ECM）成分的合成。结果，高葡萄糖诱导的DAG / PKC途径的激活被抑制，这与通过COSG治疗通过GLUT2的表达控制的葡萄糖浓度有关。