effect of peroxisome proliferator - activated gamma agonist on resistin in obese rats with type 2 diabetes

Adipocytes are highly differentiated cells and numerous genes are expressed significantly in fat cells, resistin is an adipocytokine highly expressed in murine adipose tissue. Peroxisome proliferator-activated gamma agonists [PPAR] down-regulate resistin gene expression in adipose tissue. The aim of the present work is to clarify the effect of peroxisome proliferator-activated gamma agonist [rosiglitazone] on resistin in obese rats and obese rats with type 2 diabetes. Forty eight white albino male rats of 150-250gm average weight were randomly divided into group 1: Control group [n=8], group 2: [n=8] rats received rosiglitazone, group 3s [n=32] obese rats, this group subdivided into group 3a: Obese rats recieved the drug [n=8]. Group 3b: Obese rats after induction of type 2 diabetes, Group 3c: Obese rats with diabetes and rosiglitazone [n=8]. At the time of scarification blood was collected and samples from central fat and peripheral fat was taken. The following parameters were assessed, serum glucose, triglycerides, cholesterol, insulin, serum resistin and resistin in fats. The results of the present work showed that serum glucose, insulin, triglycerides and cholesterol were significantly higher in [group 3, group 3b] compared to the control while their levels decreased after administration of the drug [Group 3c]. As regard resistin level in serum, central fat and peripheral fat were significantly higher in [group 3 and group 3b] compared to the control however its level significantly decrease after rosiglitazone administration. Also significant correlation were found between serum resistin and serum glucose, serum triglycerides and body mass index in all studied groups. Conclusion resistin seems to play an important role in development of type 2 diabetes particularly on top of obesity and its response to [PPAR] agonist may be used to relive insulin resistance in type 2 diabetes

Gene expression of vasopressin receptor type 2 and aquaporin 2 in acute renal failure versus chronic renal failure in rats

Urinary concentration decreases in response to a reduction of functioning renal mass. Although a variety of factors have been implicated, the pathogenesis of impaired urinary concentration ability in acute renal failure [ARF] and in chronic renal failure [CRF] especially the cellular and molecular defects, were poorly understood. Our study therefore aimed to present a possible explanation for the pathogenesis of impaired urinary concentration and the molecular defect in kidney tissue of experimental ARF and CRF rat models and aimed to find and compare any molecular defect difference between ARF and CRF. Thirty albino adult male rats were used in our study and the animals were divided into three groups. Group I: Sham-operated controls [n=10]. Group II: Renal ischemia-reperfusion injury group [n=10] in which the renal artery and vein were bilaterally exposed and occluded for 30min with vascular clamps to produce renal ischemia-induced acute renal failure [ARF], the clamps were removed to allow kidney reperfusion then the animal sacrified after 24H. Group III: Chronic renal failure group [n=10], this group of animals underwent right total nephrectomy and removal of 2/3 of the left kidney and the experimental protocol lasted about one month then the animals were sacrified. Blood, urine and kidney tissue samples were collected from the three groups to measure serum urea and creatinine and 24 hour-urinary albumin for evaluation of kidney function and to measure aquaporin 2 water channel and vasopressin-receptor type 2 [V[2]] gene expressions in kidney tissue. Kidney function tests as regards serum urea, serum creatinine and 24 hour-urinary albumin in group II and group III showed a significant [p<0.05] increase in comparison to control group [group I]. Ischemic-reperfusion rats [group II] showed the highest of these parameters indicating that, they had the worst kidney function. A significant [p<0.05] decrease in vasopressin-receptor type 2 [V[2]] mRNA expression in kidney tissue was shown in group II [ARF] and group III in comparison to the control rats [group I] with the highest reduction in group II. A similar result was found as regards Aquaporin 2 water channel mRNA expression with a significant [p<0.05] reduction in group II and group III in comparison to group I, and the highest reduction was seen in group II among the three studied groups. In both ischemia-reperfusion rats and CRF rats, the ischemic and nephrectomy insults were associated with decreased mRNA expression of the aquaporin 2 and vasopressin-receptors type 2 [V[2]] in the kidney tissue, coinciding with the impairment of kidney function. This may contribute to the impairment in urinary concentration in the post-ischemic period and the urinary concentration defect associated with CRF