An inhibitor of a-amylase was isolated and purified from an extract of white kidney beans (Phaseolus vulgaris). The acute oral administration of the inhibitor (50 mg/kg body weight) to adult Wistar rats together with a starch load (2 g/kg body weight suspended in NaCl (9 g/l)) reduced the increase in glycaemia over the basal value (NaCl, 222 (SEM 49); inhibitor, 145 (SEM 16) mmol/l £ 180 min; P, 0·05) without modifying the insulin response. On administering the inhibitor orally (50 mg/kg body weight dissolved in NaCl (9 g/l)) for 21 d to rats fed on a standard diet, a decline was observed in the glycaemia values on day 0 (NaCl, 5·53 (SEM 0·12); inhibitor, 5·25 (SEM 0·16) mmol/l) relative to those obtained on days 10 (NaCl, 5·00 (SEM 0·14); inhibitor, 4·60 (SEM 0·08) mmol/l; P,0·05) and 21 (NaCl, 5·22 (SEM 0·22); inhibitor, 4·50 (SEM 0·12) mmol/l; P,0·01) of treatment, without modifying the plasma concentration of insulin. There was found to be a significant anorexigenic action of the inhibitor; there was reduced food intake (NaCl, 23·07 (SEM 0·31); inhibitor, 19·50 (SEM 0·49) g/ d; P,0·01), a reduced weight gain (NaCl, 52 (SEM 3); inhibitor, 2 1·33 (SEM 8·9) g/21 d; P, 0·01), as well as changes in the activity of some intestinal enzymes such as maltase (NaCl, 87 (SEM 7); inhibitor, 127 (SEM 11) U/g proteins; P,0·05). The present study has shown, for the first time, that the prolonged administration of an a-amylase inhibitor reduces blood glucose levels and body-weight gain in Wistar rats.a-Amylase inhibitor: Glycaemia: Weight: Food intake: Disaccharidases

Summary. Many studies have shown that experimental type 1 diabetes causes morphological, functional, and metabolic alterations in the small intestine. The more frequent form of the disease, type 2 diabetes, however, has been less studied. Here the influence of diabetes on the functionality of the small intestine was studied in an experimental diabetes model, with a certain degree of residual insulin secretion, specifically in the n0-STZ model. - The diabetic rats in this model were found to have glycaemia levels higher than in the controls (8.82 +/- 0.27 and 6.18 +/- 0.18 mmol/L; p < 0.01), while their plasma insulin levels were lower than in the control rats (2.65 +/- 0.32 and 3.60 +/- 0.25 ng/ml; p < 0.05). Although there were no significant variations in body weight between the two groups, both the weight and the length of the intestine were significantly greater (p < 0.05) in the diabetic rats than in the controls. The sucrase and maltase activities were greater (p < 0.01) in the proximal intestine of the diabetic rats (94 +/- 8 and 234 +/- 12 mU/mg protein, respectively) than in the control rats (50 +/- 2 and 149 +/- 20 mU/mg protein, respectively). The 6-phosphofructo-1-kinase activity (mU/mg proteins) was less (p < 0.05) in the proximal and distal intestine of the diabetic rats (160 +/- 40 and 80 +/- 20, respectively) than in the controls (280 +/- 30 and 230 +/- 30, respectively). No significant differences were observed in the lactate dehydrogenase or active and total pyruvate dehydrogenase measured in the distal and proximal intestine of control and diabetic rats. In conclusion, our results show that experimental diabetes (n0-STZ model) similar to human type 2 diabetes produces certain morphological and enzymatic alterations which affect the digestion and absorption of carbohydrates and the intestinal metabolism of glucose. These alterations may contribute to producing the post-prandial hyperglycaemia which characterizes diabetes.