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INTRODUCTION: Insulin Resistance is a major cause of Atherosclerosis (AS) and Non Alcoholic Fatty Liver Disease (NAFLD). These lipid alterations in blood vessels and liver may progress to cardiovascular abnormalities and cirrhosis respectively. Drugs like pioglitazone (PIO) and metformin (MET) are effective insulin sensitizers used in T2DM. But their efficacy and tolerability needs to be compared in IR associated abnormalities. AIM: To compare the efficacy of PIO and MET in glucocorticoid induced AS, Hepatic Steatosis (HS) and IR in albino rats. MATERIALS AND METHODS: Male Wistar albino rats were randomized into four groups (n=6). Group 1 (Normal control) rats consumed 2% gum acacia orally for 12 days. Group 2 {dexamethasone (DEX) control} rats were administered 2% gum acacia orally for 12 days and DEX (8 mg/kg) intraperitoneally (i.p.) from 7th to 12th day during the study period. Group 3 and 4 (PIO and MET control) rats received oral administration of PIO (45 mg/kg) and MET (1000 mg/kg) for 12 days respectively. Both groups were treated with DEX (8 mg/kg/i.p.) from 7th to 12th day during the study period. On last day, fasting blood was collected and rats were sacrificed by cervical dislocation; aorta and liver tissues were isolated for the histopathological examination. Body weight, liver weight and liver volume were measured. Blood samples were processed for biochemical parameters. The data were analysed by One-way Analysis of variance (ANOVA) followed by Scheffe's multiple comparison post-hoc test. The statistical significance was assumed at p<0.05. RESULTS: Our results established the possible role of DEX in the development of AS and HS. Histopathological examination of Group 2 rats treated with DEX showed a marked lipid accumulation in the aorta and liver. Administration of MET and PIO resulted in partial to complete restoration of DEX induced fatty changes in aorta and liver. Both drugs significantly (p<0.05) prevented the elevation of insulin, lipid, glucose levels, liver weight and liver volume in DEX treated rats. They had significantly (p<0.05) improved body weight and insulin sensitivity. However, PIO was highly significant (p<0.05) compared to MET in reducing DEX induced IR complications. CONCLUSION: These findings suggest that PIO was more effective insulin sensitizer compared to MET in reducing AS, HS and IR induced by glucocorticoids.
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INTRODUCTION: Antioxidants are reported to have antiulcer activity. We investigated silymarin, a bioflavonoid antioxidant, for antiulcer potential. MATERIALS AND METHODS: Pylorus-ligated Shay rats (n=5) were used as the experimental gastric ulcer animal model. The rats, separated into three groups, were administrated silymarin (50 mg/kg), omeprazole (3.6 mg/kg), or saline (5 ml/kg) per orally daily for 5 days prior to ulcerogenic challenge. Nineteen hours after the challenge, the rats were sacrificed and their stomachs isolated. Formed gastric juice was collected for measurement of volume, titrimetric estimation of free and total acidity, and total acid output by the conventional methods. The ulcer index was calculated. Total acid output and free and combined acid quantities were calculated using the acidity value and the volume of formed gastric juice. RESULTS: Silymarin exerted significant (P<.05) antiulcer activity (the ulcer index was reduced to 7.4 ± 1.0 from the control value of 19.8 ± 4.1). Silymarin also significantly reduced free and total acidity, gastric juice volume, total acid output, and combined acid content. The results were analyzed by ANOVA and Newman-Keuls multiple comparison test. CONCLUSION: This study demonstrates that silymarin has significant antiulcer activity. It perhaps acts by decreasing hydrochloric acid output and increasing buffering power (combined acid).