Improvement of insulin resistance via increase of GLUT4 and PPARγ in metabolic syndrome-induced rats treated with omega-3 fatty acid or l-carnitine.

BACKGROUND: Frequent consumption of fructose and saturated fatty acids increase risk of metabolic syndrome (MS). Features of MS include insulin resistance, dyslipidemia, visceral obesity, and hypertension. The aim of this study was to investigate the role of omega-3 and l-carnitine in ameliorating features of MS. METHODS: MS was induced in rats by high-fructose high-fat fed diet for 8 weeks. They were randomly divided into five groups: normal control, MS control group treated with saline, MS groups given omega-3 (260 mg/kg), l-carnitine (200 mg/kg), or metformin (100 mg/kg) daily for 4 weeks. Body weight, relative organ weight, glucose, insulin, adiponectin, and lipid profiles were estimated. Also glucose transporter 4 (GLUT4) content and peroxisome proliferator-activated receptor-gamma (PPARγ) protein expressions were determined. RESULTS: Omega-3 and l-carnitine caused decrease in both MS-induced increase in body weight and glucose similar to metformin. They reduced insulin level and resistance with increased adiponectin, and correction of MS-induced hyperlipidemia. Drugs also increased GLUT4 and PPARγ protein expression compared with MS control group. CONCLUSION: Omega-3 and l-carnitine improve features of MS via increased GLUT4 and PPARγ expression.

Hesperidin and rutin, antioxidant citrus flavonoids, attenuate cisplatin-induced nephrotoxicity in rats.

This study aimed to assess the protective effect of hesperidin (HES) and rutin (RUT) against cisplatin-induced nephrotoxicity in male rats. Cisplatin (5 mg/kg, intraperitoneal) caused significant increases in serum sodium, blood urea nitrogen, serum creatinine, total sodium and potassium excreted in urine, urine volume, and lipid peroxides measured as the malondialdehyde content of kidney, with significant decreases in serum total protein, creatinine clearance, reduced glutathione content of kidney, and kidney superoxide dismutase activity as compared with the control group. On the other hand, administration of HES (200 mg/kg, per oral [p.o.]) or RUT (30 mg/kg, p.o.) for 14 days with a single cisplatin dose on the tenth day ameliorated the cisplatin-induced nephrotoxicity as indicated by the restoration of kidney function and oxidative stress biomarkers. Furthermore, the test drugs reduced the histopathological changes induced by cisplatin. In conclusion, HES and RUT showed protective effects against cisplatin-induced nephrotoxicity.

Pharmacological study of the effect of licorice alone and in combination with diclofenac sodium on hepatotoxicity-induced experimentally in rats.

The protective effect of licorice and diclofenac sodium in doses of 50 mg/kg bwt. and 5 mg/kg bwt. respectively against liver toxicity induced by CCl4 (1ml/kg bwt.) in olive oil [1:1 (v/v)] every other day for 8 weeks and by hepatic ischemia/reperfusion in adult male albino rats was studied. Different antioxidant and liver function parameters were reported to find the protective effect of both licorice and diclofenac sodium against hepatotoxicity. Results showed that licorice protected against CCl4-induced hepatotoxicity as well as ischemia/reperfusion-induced liver injury. On the other hand, diclofenac sodium caused deleterious effects, especially in presence of CCl4, where a high mortality rate was observed.