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Aim: Increase in blood glucose level has been associated with beta cells destruction which is enhanced by lipid peroxidation and hepatocellular damage. The present study was designed to investigate the effect of oral administration of theophylline on Liver enzymes (ALT, AST and ALP) and Liver histology in alloxan-induced diabetic male wistar rats.
Study Design: This is an experimental study. Thirty healthy male wistar rats weighing between 160-180 g were grouped into five of six animals each (n=6) following the induction hyperglycaemia using alloxan monohydrate and treated for a period of fourteen days (14) as follows; Group 1: (Normoglycaemic) Group 2: Diabetic control, Group 3: Glibenclamide, 5mg/kg, Groups 4 and 5; theophylline 5mg/kg and 10mg/kg respectively. At the end of the experiment, blood samples were taken from all treated groups and sera obtained. Serum levels of ALT, AST and ALP were measured. Liver tissues were also harvested from experimental groups, and histological assessment carried out.
Results: There were no statistically significant differences observed in serum ALP, ALT and AST levels in the theophylline treated groups compared to the diabetic control. The levels of ALP and ALT were however significantly higher (P< 0.05) in the theophylline treated groups than that observed in the glibenclamide treated group. Serum levels of ALP and ALT were significantly lowered (P< 0.05) in the glibenclamide treated group compared to both the diabetic control and the theophylline treated groups. Although less fatty infiltrations and hepatocellular degeneration were observed in the liver tissues of theophylline and glibenclamide treated groups compared to diabetic control, the effect was more in the glibenclamide treated group compared to the theophylline treated groups.
Conclusion: In this study, glibenclamide recorded less hepatotoxic activity by significantly lowering serum liver enzymes; ALP and ALT in contrast to theophylline which showed no significant differences in levels of serum enzymes in alloxan induced hyperglycaemic rats.