Objective To observe the morphologic changes of pancreatic islets in diabetic rats and the protective effects of rosiglitazone natrium (RSG) on the remnant islet.Methods 8 rats were randomly selected from 68 male Sprague-Dawley rats for normal control group (group A),the rest were administered with STZ,and those with FBG≥16.7mmol/L were served as diabetic models,then the rats were randomly assigned as RSG-treated group (group B,n=24).RSG were applied via intragastric administration at a dose of 5mg/(kg·d) in group B.72 hours after the administration of STZ and 1-,2-,4 and 7 week after the administration of RSG,4 rats were randomly selected respectively,pancreas specimens were obtained and preserved.The morphologie changes were observed under light microscopes and transmission electron microscope.Results The diabetic symptoms of the rats in groupe B lessened significantly,and the FBG levels were decreased gradually,the morphologic injuries of remnant islet were recovering. The amount of secretory granule in beta cells increased gradually.Conclusion Rosiglitazone natrium call attenuate morphologic injuries of the islets and protect the remnant islet in type 1 diabetes mellilus rats.

Objective To investigate the effects of rosiglitazone on tree shrew's fatty liver induced by high sugar and fat diet. Methods Thirty six tree shrews were assigned as the chow diet group (group A, 8 animals) and the high sugar and high fat fed group (28 animals). The latter were fed alternately with the mix food containing 40% saccharu and 20% fat by one day interval. In the high sugar and high fat fed group, 19 animals (67.86%), which had an increased FBG level equal to or more than 11.1 mmol/L 22 weeks after the diet, were divided into 2 subgroups: rosiglitazone supplemented group (group B), to which rosiglitazone was added at a dose of 5 mg?kg -1 ?d -1 for seven weeks, and non supplemented group (group C). Body weight, fasting serum insulin(FINS) and blood lipid including total cholesterol(TC), triglyceride (TG), high density lipoprotein cholesterol (HDL C) and low density lipoprotein cholesterol (LDL C) were examined during the experiment. Liver biopsies were carried out under general anaesthesia at 22 week and the end of the experiment in all animals. The samples of liver were fixed in 4% polymerisatum for 12 h, then through pathological routine processing. The expressions of uncoupling protein 3 (UCP3) and insulin receptor (IR) were analyzed by calculating the UCP3 and IR expressing positive cells and by analyzing the area density of positive cells using computer aided video system. Results Morphological alteration under light microscopy showed that all animals from both group B and C had a typical steatosis throughout the liver sections 22 week after high sugar and high fat feeding. The area density of steatosis and the proportion of involved hepatocytes were approximately 30% and reached higher degrees in group C ( P 0.05) .Conclusion Increased expression of liver for IR ? in tree shrews on a high sugar and high fat diet indicates that insulin signaling may have a role in the development of hepatosteatosis.

Objective To investigate the effect of smoking and smoking cessation on the phosphorylation of IKK-β in type 2 diabetic rats. Methods Forty-two six-week-old Wistar rats were randomly divided into 4 groups: normal control(NC, n =7), diabetes control (DC, n =7), diabetes with smoking (DS, n = 14) and diabetes with smoking cessation(SC, n = 14). Rats in DS and SC groups were further assigned randomly into 8w and 12w subgroups. DS group was given passive smoking twice a day for 8 or 12 weeks, while SC group ceased passive smoking for 4 weeks after 8 or 12 weeks of smoking . Western blot method was used to detect the level of IKK-13 phosphorylation in skeletal muscle. Results Compared with the NC group,the phosphorylation of IKK-β protein in DC group was increased (0. 16±0. 05 vs 0. 30±0. 08, P < 0. 01). There was an increasing trend with the phosphorylation level of IKK-β in the DS (8w) subgroup, but there was no statistical difference between the DC group and SC(8w) subgroup (0. 40±0. 09 vs 0. 30±0. 08,0. 36±0. 10, P >0. 05). The phosphorylation level of IKK-β in DS(12w) group increased obviously, being significantly higher than that in the DC group and SC (12w) subgroup(0. 74 ± 0. 11 vs 0.30±0.08,0.35±0.07,P < 0.01). Conclusion With the prolongation of smoking duration, the phosphorylation of IKK-β in type 2 diabetic rats increased. After smoking cessation, the phosphorylation of IKK-β decreased. The phosphorylation of IKK-β may be involved in the mechanism by which smoking causes type 2 diabetes.