Rocío Bautista

Sodium-Glucose Cotransporter Inhibition Prevents Oxidative Stress in the Kidney of Diabetic Rats

The hyperglycemia triggers several chronic diabetic complications mediated by increased oxidative stress that eventually causes diabetic nephropathy. The aim of this study was to examine if the sodium-glucose cotransporter (SGLT2) inhibition prevents the oxidative stress in the kidney of diabetic rats. Methods. The diabetic rat model was established by intraperitoneal injection of streptozotocin (50 mg/kg). The inhibition of SGLT2 was induced by daily subcutaneous administration of phlorizin (0.4 g/kg). Oxidative stress was assessed by catalase (CAT), glutathione peroxidase (GPx), and superoxide dismutase (SOD) activities and by immunohistochemical analysis of 3-nitrotyrosine (3-NT). Results. Streptozotocin-induced diabetes caused hyperglycemia and lower body weight. The CAT activity decreased in cortex and medulla from diabetic rats; in contrast, the GPx activity increased. Furthermore the 3-NT staining of kidney from diabetic rats increased compared to control rats. The inhibition of SGLT2 decreased hyperglycemia. However, significant diuresis and glucosuria remain in diabetic rats. The phlorizin treatment restores the CAT and GPX activities and decreases 3-NT staining. Conclusion. The inhibition of SGLT2 by phlorizin prevents the hyperglycemia and oxidative stress in kidney of diabetic rats, suggesting a prooxidative mechanism related to SGLT2 activity.

Effect of treatment with losartan on salt sensitivity and SGLT2 expression in hypertensive diabetic rats

Sodium-glucose cotransporters (SGLTs) in the kidney, may be involved in hypertension, diabetes and salt sensitivity. We evaluate the effect of losartan on blood pressure (BP) and SGLT2 expression in diabetic rats with high or normal salt diet. Losartan prevented an increase in BP and SGLT2 expression in diabetic rats.

Ursodeoxycholic acid decreases sodium-glucose cotransporter (SGLT2) expression and oxidative stress in the kidney of diabetic rats

UNLABELLED Oxidative stress has been associated with diabetic complications like nephropathies. Recent studies indicate that ursodeoxycholic acid (UDCA) may be beneficial preventing diabetes-induced oxidative stress and secondary complications. Thus, we study if the UDCA-treatment decreases the expression of sodium-glucose cotransporter (SGLT2) and the oxidative stress in the kidney of diabetic rats. METHODS The diabetes model was established by intraperitoneal injection of streptozotocin (50mg/kg). SGLT2 expression was evaluated by western blot and RT-PCR. Oxidative stress was assessed by catalase (CAT), glutathione peroxidase (GPx) and superoxide dismutase activities (SOD) and immunohistochemical analysis of 3-nitrotyrosine (3-NT). RESULTS Streptozotocin-induced diabetes caused hyperglycemia and lower body weight. The SGLT2 expression and mRNA levels increased in cortex of kidney from diabetic rats. The CAT activity decreased in cortex and medulla from diabetic rats, otherwise the GPx activity increased. Furthermore the 3-NT staining of kidney from diabetic rats increased compared to control rats. The UDCA treatment was able to decrease hyperglycemia and prevents the SGLT2 over-expression, restores the CAT and GPX activities and decreases 3-NT staining. CONCLUSION The UDCA treatment prevents the over-expression of SGLT2 and oxidative stress in kidney of diabetic rats.

Early endothelial nitrosylation and increased abdominal adiposity in Wistar rats after long-term consumption of food fried in canola oil

OBJECTIVE The aim of this study was to establish whether the long-term consumption of reused canola oil contributes to the development of dyslipidemia, obesity, and endothelial function. METHODS Canola oil was used for one frying cycle (1 FC) of corn flour dough or reused 10 times (10 FC). Rats received chow diet (control) or supplemented with 7% raw oil (RO), 1 FC or 10 FC oil (n = 10 per group). Food consumption, blood pressure (BP), and body weight plasma glucose, plasma lipids were monitored. Vascular reactivity was analyzed using aorta rings stimulated with phenylephrine and acetylcholine. Nitrotyrosine presence in aorta rings was analyzed by immunohistochemistry. RESULTS After 10 wk of follow-up, visceral adipose tissue was significantly more abundant in 1 FC (7.4 ± 0.6 g) and 10 FC (8.8 ± 0.7 g) than the RO (5.0 ± 0.2 g; P = 0.05 versus 10 FC group) or control group (2.6 ± 0.3 g; P = 0.05 versus all groups). Despite similar plasma cholesterol, triglycerides, and BP among groups, a significantly reduced acetylcholine-induced vascular relaxation was observed in the three groups receiving the oil-supplemented diet (47.2% ± 3.6%, 27.2% ± 7.7%, and 25.9% ± 7.6% of relaxation, for the RO, 1 FC, and 10 FC, respectively; P < 0.05 for all versus 62.4% ± 9.7% of the control group). Endothelial dysfunction was concomitant with the presence of nitrotyrosine residues at a higher extent in the groups that received heated oils compared with the RO group. CONCLUSION High canola oil intake over 10 wk was associated with increased adipose tissue and early endothelial dysfunction probably induced by peroxinitrite formation. Such deleterious effects were significantly potentiated when the consumed oil had been used repeatedly for frying.