ABSTRACT
Diabetic complications may in part be due to inflammation. Diabetes can also develop in non-obese people.Nonetheless, organ inflammation in non-obese type 2 diabetes mellitus animals has never been investigated. The GotoKakizaki rats were divided into two groups: diabetes and diabetes treated with metformin. The glycemia parameterswere then determined. Serum and internal organs, including the liver, kidney, and brain were collected to determinethe levels of inflammatory cytokine and mRNA expression. The research found an increase in interleukin-6 (IL-6)and IL-1β cytokine levels in the liver of the diabetic group, which corresponds with the mRNA expression of bothcytokines. The metformin group significantly reduces the mRNA expression of liver IL-6. In the kidney, there was anincrease in IL-6 cytokine levels in the diabetic group, while the metformin group could reduce the mRNA expressionlevel of tumor necrosis factor α (TNF-α). In addition, there were IL-6 and TNF-α cytokines level increased in thebrain of the diabetic group. IL-1β mRNA expression levels increased in the diabetic group and were reduced by themetformin treatment. The metformin treatment reduced serum TNF-α cytokines. In summary, this study demonstratedthat internal organ inflammation in non-obese diabetic rats, which could provide evidence for organ inflammation,may potentially explain diabetic complications.
ABSTRACT
Diabetic complications may in part be due to inflammation. Diabetes can also develop in non-obese people.Nonetheless, organ inflammation in non-obese type 2 diabetes mellitus animals has never been investigated. The GotoKakizaki rats were divided into two groups: diabetes and diabetes treated with metformin. The glycemia parameterswere then determined. Serum and internal organs, including the liver, kidney, and brain were collected to determinethe levels of inflammatory cytokine and mRNA expression. The research found an increase in interleukin-6 (IL-6)and IL-1β cytokine levels in the liver of the diabetic group, which corresponds with the mRNA expression of bothcytokines. The metformin group significantly reduces the mRNA expression of liver IL-6. In the kidney, there was anincrease in IL-6 cytokine levels in the diabetic group, while the metformin group could reduce the mRNA expressionlevel of tumor necrosis factor α (TNF-α). In addition, there were IL-6 and TNF-α cytokines level increased in thebrain of the diabetic group. IL-1β mRNA expression levels increased in the diabetic group and were reduced by themetformin treatment. The metformin treatment reduced serum TNF-α cytokines. In summary, this study demonstratedthat internal organ inflammation in non-obese diabetic rats, which could provide evidence for organ inflammation,may potentially explain diabetic complications.
ABSTRACT
Aim To observe the effect of agiophyllum oligo saccharides ( AOS) on reducing blood sugar, im-proving insulin resistance on diadetic Goto-Kakizaki ( GK) rats, and to explore the possible mechanism. Methods The type 2 diabetes GK rats were divided into six groups: model control group ( MC ) , Glenn benzene urea group ( GLB ) , high agriophyllum squar-rosum coarse oligosaccharides ( AOS-H ) , medium ( AOS-M ) , low dose group ( AOS-L ) , homologous Wistar rats as normal control ( NC ) . All animals were administered with AOS by oral gavage, for 8 weeks. The fasting blood glucose ( FBG) , random blood sugar ( RBG) , glucose tolerance ( OGTT) were tested before and after administration. No fasting sugar load status before and after dosing changes in blood glucose and serum insulin level in rats were measured in the previ-ous 8 weeks. At the end of administration, the fasting serum glucose ( FPG) , insulin ( FINS) , OGTT and in-sulin resistance index ( HOMA IR) in fasting rats were analyzed. Lastly, the pathological changing of pancreas was observed by HE staining. Results The blood glucose of fasting GK rats was not influenced after using AOS. However, the random blood glucose significantly reduced, the glucose tolerance was improved and AUC was obviously reduced (P < 0. 01) after using AOS. The best effect was on AOS-M group, which was similar with Glenn benzene urea. Through our research, we found AOS could promote release of insulin. This best effect was on AOS-M and AOS-L groups, and the time and quantity of release were better than Glenn benzene urea. Finally, AOS inhibited the pathological changes of islet tissue on GK rats, increased the quantity of pancreas and islet cells. Compared with model group, the changing of islet structure was significantly reduced in AOS group. Conclusion AOS could obviously improve insulin resistance and lower blood sugar, and the mechanism of this effect may be related with rapidly promoting insulin release, increasing the islet cell proliferation,and improving the function of islet.
ABSTRACT
Objective To investigate the therapeutic effects and mechanism of biliopancreatic diversion (BPD) surgery on type 2 diabetes mellitus(T2DM) in GK rats.Methods 16 GK rats were randomly divided into 2 groups:BPD surgery group included 10 rats undergoing BPD surgery,sham-BPD group included 6 rats undergoing a sham operation.Fasting plasma glucose,insulin,glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide(GIP)were detected one week before BPD surgery and the 1st week,4th week,10th week,26th week after BPD surgery.Oral glucose tolerance test(OGTT) and insulin tolerance test(ITT) were done in the 10th week after BPD surgery.Results There was no statistical difference in fasting plasma glucose,insulin,plasma GLP-1 or GIP between the 2 groups before surgery.Plasma glucose had significant reduction in BPD group compared to that in the sham group(P ＜0.05) and insulin level had no significant difference between the 2 groups.Rats in BPD group had significant improvement in glucose tolerance and insulin sensitivity compared to those in the sham group.Serum level of GLP-1 was significantly elevated in BPD group compared to that before surgery (P =0.0337 at the 1st week after surgery; P =0.0002 at the 4th week after surgery,P ＜ 0.0001 at the 10th week after surgery,P ＜0.0001 at the 26th week after surgery) and that in sham-BPD group(P =0.0354 at the 1st week after surgery,P =0.0032 at the 4th week after surgery,P =0.0001 at the 10th week after surgery,P ＜0.0001 at the 26th week).Serum level of GIP was significantly lowered in BPD group compared to that before surgery(P =0.0189 at the 1st week after surgery; P =0.0007 at the 4th week after surgery,P =0.0003 at the 10th week after surgery,P ＜0.0001 at the 26th week after surgery) and that in sham-BPD group(P =0.0089 at the 1st week after surgery,P =0.0002 at the 4th week after surgery,P =0.0006 at the 10th week after surgery,P ＜0.0001 at the 26th week after surgery).The difference had statistical significance (P ＜0.05).Conclusion BPD surgery can significantly reduce fasting plasma glucose,improve glucose tolerance and insulin sensitivity.The change of serum levels of GLP-1 and GIP may play the major role in BPD treatment of diabetes mellitus.
ABSTRACT
The aim of this study was to examine the hypoglycemic effect of chlorella in 6 week-old type 2 diabetic Goto-Kakizaki (GK, n=30) rats and 6 week-old normal Wistar (n=30) rats. Animals were randomly assigned to 3 groups respectively, and were fed three different experimental diets containing 0%, 3% or 5% (w/w) chlorella for 8 weeks. In diabetic GK rats, the insulinogenic-indices were not significantly different among the groups. The concentrations of fasting plasma glucagon and hepatic triglyceride, and the insulin/glucagon ratios of the GK-3% chlorella and GK-5% chlorella groups were significantly lower than those of the GK-control group. The HOMA-index and the concentrations of fasting blood glucose and plasma insulin of the GK-3% chlorella and GK-5% chlorella groups were slightly lower than those of the GK-control group. In normal Wistar rats, the insulinogenic-indices were not significantly different among the normal groups, but that of the Wistar-5% chlorella group was slightly higher than the other groups. The concentrations of fasting blood glucose and plasma insulin, and the HOMA-index of the Wistar-5% chlorella group were a little higher, and the fasting plasma glucagon concentration and the insulin/glucagon ratio of the Wistar-5% chlorella group were significantly higher than those of the Wistar-control and Wistar-3% chlorella groups. In conclusion, this study shows that the glucose-stimulated insulin secretion was not affected by the intake of chlorella, which could be beneficial, however, in improving insulin sensitivity in type 2 diabetic GK and normal Wistar rats.