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    The effect of hydrophilic statins on adiponectin, leptin, visfatin, and vaspin levels in streptozocin-induced diabetic rats
    (Springer, 2024) Kaya, Hacer Kayhan; Demirtas, Berjan
    Statins may affect glucose metabolism through adipokines. The aim of this study was to measure the effects of hydrophilic statins on the levels of several adipokines in diabetic rats. Wistar albino rats were divided into four groups: healthy control, untreated diabetic, diabetic treated with pravastatin, and diabetic treated with rosuvastatin. Diabetes was induced by intraperitoneal injection of STZ. Thereafter, 20 mg/kg/day doses of either pravastatin or rosuvastatin were administered to the treated diabetic rats for 8 weeks. At the end of the experiment, the body weights, fasting blood glucose levels, serum insulin levels, and insulin resistance, as well as the serum adiponectin, leptin, visfatin, and vaspin levels, were measured. Fasting blood glucose and insulin resistance levels were significantly higher, whereas insulin levels and body weight were significantly lower in the untreated diabetic group than in the control group. Diabetes caused significant decreases in adiponectin, leptin, and vaspin levels but a significant increase in visfatin levels. Pravastatin treatment significantly increased body weight and decreased fasting blood glucose levels, whereas rosuvastatin decreased body weight but did not affect fasting blood glucose levels. Pravastatin caused significant increases in both adiponectin and vaspin levels. However, rosuvastatin did not affect the adiponectin level but caused a significant decrease in the vaspin levels. Both pravastatin and rosuvastatin treatments decreased the leptin and visfatin levels. In conclusion, pravastatin is more effective at improving fasting blood glucose levels and body weight in diabetic rats, probably by increasing adiponectin and vaspin levels.
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    Effect of Kefir Consumption on Erythrocyte Osmotic Fragility and Some Haemetological Parameters in Smokers and Non-Smokers
    (Wiley, 2017) Diken, Huda; Oguz, Zelal; Kaya, Hacer; Demirtas, Berjan; Kelle, Mustafa; Atmaca, Mukadder
    [Abstract Not Available]
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    Influence of coumarin and some coumarin derivatives on serum lipid profiles in carbontetrachloride-exposed rats
    (Sage Publications Ltd, 2017) Tasdemir, Ezel; Atmaca, Mukadder; Yildirim, Yasar; Bilgin, Hakki Murat; Demirtas, Berjan; Obay, Basra Deniz; Kelle, Mustafa
    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.