Study of the Hypoglycemic Effect of Tamarindus indica Linn. Seeds on Non-Diabetic and Diabetic Model Rats.

ABSTRACT

Aim: The present study was undertaken to evaluate the antidiabetic effects of the Tamarindus indica Linn seed in normal (non-diabetic), type-I and type-II model rats and to investigate their effect on gastrointestinal motility and intestinal glucose absorption. Methodology: T. indica seed powder was used at a dose of 1.25g/kg bw/10 ml water. Male Long-Evans rats (160-210g body weight) were used for the experiment. Experiments were done in non-diabetic and streptozotocin-induced diabetic model rats with a single feeding in different prandial states and blood was collected. An intestinal perfusion technique was used to study the effects of T. indica seed powder on intestinal glucose absorption in normal and type-II model rats. Gut motility was evaluated using barium sulfate milk. Glucose was measured by Glucose oxidase-peroxidase (GOD-POD) method. Result: The screening results showed that T. indica seed powder had no effect on fasting or postprandial serum glucose level of normal and type-I diabetic rat. The seed powder also showed no hypoglycemic effect in the fasting state and no antihyperglycemic effect in type-II model rats when fed simultaneously with oral glucose load, but it exhibited significant antihyperglycemic effect when the seed powder was fed 30 minutes prior to the glucose load at 105 minutes (p<0.03). Glibenclamide significantly lowered postprandial serum glucose levels of non-diabetic and type-II diabetic model rats (p<0.02-0.001). T. indica exerted inhibition on glucose absorption in type-II rats during the whole perfusion period when compared with control. On the other hand, T. indica seed powder significantly inhibited the gastrointestinal motility in type-II rats. Conclusion: The present data suggest that T. indica possesses antihyperglycemic properties in type-II rats which are at least partly due to its inhibitory effect on intestinal glucose absorption. This effect cannot be attributed to the acceleration of intestinal transit.