Search

To develop a convenient animal model of T2D by pretreatment with low-dose 10% w/v fructose (FRC) solution followed by the injection of low doses of streptozotocin (STZ) in Wistar rats. For this 8-week experimental study; rats were first fed a standard chow ad-libitum diet and either tap water (n=40) or 10% w/v FRC solution (n=40) for 4 weeks. Next, rats in each category were randomly allocated to 4 subgroups (n=10 each) of low-dose STZ (25,35, and 45 mg/kg). The final mean fasting blood sugar (FBG) of FRC+STZ45 (197±55.87 mg/dl) were significantly higher than that of the STZ45 (P=0.015) and FRC (P=0.019) groups. FRC+STZ45 showed the highest insulin resistance demonstrated by insulin tolerance test [area under the curve (AUC) of insulin tolerance test; P<0.05]. AUC was not significantly different between the STZ45 and non-STZ groups and between FRC and non-FRC fed groups. Furthermore, FBG levels did not differ between FRC and non-FRC groups. Body weight measurement showed that the FRC+STZ45 group had the lowest body weight compared to all other groups. Our data provide the evidence that FRC and STZ45 synergistically could induce hyperglycemia and insulin resistance in Wistar rats. Here we presented a feasible model for initial forms of T2D by employing pretreatment with low-dose FRC solution and treatment with low-dose STZ. [ABSTRACT FROM AUTHOR]

Objectives : The role of miR-155 in immune responses of PBMCs of type 2 diabetic (T2D) patients has not been studied. Design and methods : 20 Healthy and 20 T2D subjects were participated in the study. miR-155 expression in PBMCs of the subjects was measured using real-time PCR. The levels of secreted IL-6 and TNF-α cytokines were quantified using ELISA. Results : A downregulation of miR-155 expression was observed in untreated and LPS treated PBMCs of diabetic patients compared to controls. There was a significant upregulation of miR-155 after LPS treatment in PBMCs of both control and diabetic groups. In healthy subjects and in both untreated and LPS-treated conditions, miR-155 expression was negatively correlated with weight, waist circumference and body mass index. In diabetic group, there was a negative correlation between miR-155 expression and glucose levels only in LPS treated cells. Furthermore, systolic blood pressure was found to negatively correlate with miR-155 expression in untreated PBMCs of both healthy and diabetic subjects. The results also showed a significant correlation between miR-155 expression and TNF-α and IL-6 levels in LPS treated cells. Conclusions : Our data demonstrate that miR-155 expression is reduced in PBMCs of diabetic patients and this reduced expression does not seem to be involved in increased cytokine production from PBMCs of these patients. [ABSTRACT FROM AUTHOR]