Protective potential of Averrhoa bilimbi fruits in ameliorating the hepatic key enzymes in streptozotocin-induced diabetic rats.
Ključne riječi
Sažetak
UNASSIGNED
Diabetes is a mutifactorial disease which leads to several complications. Currently available drug regimens for management of diabetes have certain drawbacks. Need for safer and effective medicines from natural sources having potent antidiabetic activity. Averrhoa bilimbi Linn. (Oxalidaceae) is a medicinal plant and is reported to possess hypoglycemic activity.
OBJECTIVE
To investigate the antidiabetic potential of Averrhoa bilimbi fruit extract in streptozotocin-induced diabetic rats.
METHODS
Diabetes was induced in male Sprague Dawley rats by single intraperitoneal injection of streptozotocin (STZ) (40mg/kg body weight). The diabetic rats were treated orally with ethyl acetate fraction of A. bilimbi fruits (ABE) (25mg/kg body weight) and metformin (100mg/kg body weight) by intragastric intubation for 60days. After 60days, the rats were sacrificed; blood, liver and pancreas were collected. Several indices such as blood glucose, plasma insulin, toxicity markers and the activities of carbohydrate-metabolizing enzymes were assayed. The phytochemicals present in the ABE was identified by gas chromatography-mass spectrometry analysis.
RESULTS
ABE significantly (p<0.05) reduced the level of blood glucose and hepatic toxicity markers and increased plasma insulin in diabetic rats. ABE modulated the activities of carbohydrate-metabolizing enzymes, significantly increased the activities of hexokinase (59%) and pyruvate kinase (68%) and reduced the activities of glucose-6-phosphatase (32%) and fructose-1, 6-bisphosphatase (20%). The histological studies of the pancreas also supported our findings. The results were compared with metformin, a standard oral hypoglycemic drug. GC-MS analysis of ABE revealed the presence of 11 chemical constituents in the extract.
CONCLUSIONS
ABE exerts its antidiabetic effect by promoting glucose metabolism via glycolysis and inhibiting hepatic endogenous glucose production via gluconeogenesis.
