Comparative effects of pravastatin and rosuvastatin on carbohydrate metabolism in an experimental diabetic rat model.

Statin treatment may increase the risk of diabetes; there is insufficient data on how statins affect glucose regulation and glycemic control and the effects of statins on liver enzymes related to carbohydrate metabolism have not been fully studied. Therefore, we aimed to compare the effects of the statin derivatives, pravastatin, and rosuvastatin, on carbohydrate metabolism in an experimental diabetic rat model. Female Wistar albino rats were used and diabetes was induced by intraperitoneal injection of streptozotocin. Thereafter, 10 and 20 mg kg-1 day-1 doses of both pravastatin and rosuvastatin were administered by oral gavage to the diabetic rats for 8 weeks. At the end of the experiment, body masses, the levels of fasting blood glucose, serum insulin, insulin resistance (HOMA-IR), liver glycogen, and liver enzymes related to carbohydrate metabolism were measured. Both doses of pravastatin significantly in creased the body mass in diabetic rats, however, rosuvastatin, especially at the dose of 20 mg kg-1 day-1 reduced the body mass signi ficantly. Pravastatin, especially at a dose of 20 mg kg-1 day-1, caused significant increases in liver glycogen synthase and glucose 6-phosphate dehydrogenase levels but significant decreases in the levels of glycogen phosphorylase, lactate dehydrogenase, and glucose-6-phosphatase. Hence, pravastatin partially ameliorated the adverse changes in liver enzymes caused by diabetes and, especially at the dose of 20 mg kg-1 day-1, reduced the fasting blood glucose level and increased the liver glycogen content. However, rosuvastatin, especially at the dose of 20 mg kg-1 day-1, significantly reduced the liver glycogen synthase and pyruvate kinase levels, but increased the glycogen phosphorylase level in diabetic rats. Rosuvastatin, 20 mg kg-1 day-1 dose, caused significant decreases in the body mass and the liver glycogen content of diabetic rats. It can be concluded that pravastatin, especially at the dose of 20 mg kg-1 day-1 is more effective in ameliorating the negative effects of diabetes by modulating carbohydrate metabolism.

Tobacco smoke induces oxidative stress and alters pro-inflammatory cytokines and some trace elements in healthy indoor cats.

This study was aimed to assess oxidative stress, pro-inflammatory cytokines and some trace elements in healthy pet cats exposed to environmental tobacco smoke. Forty healthy cats were included in this study. Cats were divided in two groups: Exposed to tobacco smoke (ETS; n = 20) and non-exposed to tobacco smoke (NETS; n = 20). Blood levels of cotinine, total oxidant status (TOS), oxidative stress index (OSI), lipid hydroperoxide (LOOH), protein carbonyl (PCO), advanced oxidative protein products (AOPP), total antioxidant status (TAS), copper, zinc-superoxide dismutase (Cu, Zn-SOD), catalase (CAT), total thiol (T-SH), interferon gamma (INF-γ), tumor necrosis factor (TNF-α), interleukin ß (IL-1ß), interleukin 6 (IL-6), interleukin-8 (IL-8), inter-leukin 2 (IL-2) and iron (Fe), zinc (Zn), copper (Cu), selenium (Se) levels were measured. Hematological and biochemical parameters were also measured. Serum cotinine, TOS, OSI, PCO, AOPP and LOOH levels were higher, whereas TAS and Cu, Zn-SOD levels were lower in ETS group. In ETS group INF-γ, IL-1ß, IL-2, and IL-6 levels were higher. The Cu level was higher in ETS group. Blood reticulocyte number, serum creatinine and glucose were higher in ETS group. It could be concluded that exposure to tobacco smoke in cats impaired the oxidant/antioxidant balance and potentially triggered the release of pro-inflammatory cytokines.

Influence of coumarin and some coumarin derivatives on serum lipid profiles in carbontetrachloride-exposed rats.

In the present study, coumarin and some coumarin derivatives (esculetin, scoparone, and 4-methylumbelliferone) were investigated for their lipid-lowering effect in rats. Male Sprague-Dawley rats (150-200 g) were divided into six groups and each group comprised of five rats. Hepatic injury-dependent hyperlipidemia was induced by carbon tetrachloride (CCl4, 1.25 ml/kg). Coumarin and coumarin derivatives esculetin (35 mg/kg), scoparone (35 mg/kg), 4-methylumbelliferone (35 mg/kg), or coumarin (30 mg/kg) were administered to experimental groups at 12-h intervals. Animals received the derivatives esculetin, scoparone or 4-methylumbelliferone prior to the administration of a single toxic dose of CCl4. Serum total cholesterol (TC), triglyceride (TG), very low-density lipoprotein cholesterol (VLDL-C), and low-density lipoprotein cholesterol (LDL-C) levels significantly increased in CCl4-treated group ( p < 0.05, p < 0.01, p < 0.01, and p < 0.05, respectively), while levels of serum high-density lipoprotein cholesterol (HDL-C) decreased ( p < 0.01). 4-Methylumbelliferone had no recovery effects on serum TC levels, however, significantly prevented CCl4-induced hyperlipidemia by reducing TG and VLDL-C levels ( p < 0.05 and p < 0.05, respectively). In addition, coumarin had no recovery effect on any of the serum lipid parameters against CCl4-induced hyperlipidemia. Among the coumarin derivatives only esculetin and scoparone significantly prevented serum HDL-C in CCl4-induced dyslipidemia. The results from this study indicate that the chemical structure of coumarins plays an important role on the regulation of serum lipid profiles.