An alpha-glucosidase inhibitor, @entity48103 , retards XXXX absorption in @entity35 and @entity1 .

@entity1 @entity48103 @entity3884 @entity11884 @entity6 @entity1735 @entity969 @entity3190 @entity35 @entity4854 @entity413
The present study was designed to determine the possible significance of a therapeutic dose (0.2 mg) of @entity48103 on @entity1735 absorption by measuring the breath @entity3884 concentration, which is an index of the amount of unabsorbed @entity1735 in the large intestine. Post-prandial @entity4854 is common among @entity6 @entity1 . @entity48103 , a potent alpha-glucosidase inhibitor, suppressed post-prandial @entity4854 and @entity3190 in healthy volunteers at a dose of 0.2 mg with each meal. These volunteers increased the breath @entity3884 concentration in response to ingestion of non-absorbable @entity11884 , but decreased only slightly its concentration from the basal level after @entity969 ingestion, indicating complete absorption. When @entity48103 (0.2 mg) was given with @entity969 , @entity3884 production increased only slightly compared with placebo, suggesting that the inhibitory effect of @entity48103 on @entity969 absorption was minimal. Only 5 g of the 100 g of @entity969 was not absorbed and this 5% reduction is too small to explain the observed inhibitory effect on the post-prandial rise in plasma @entity413 . @entity969 loading in @entity35 (about 443 mg) sharply increased blood @entity413 and was accompanied by the rapid disappearance of @entity969 from the upper small intestine. @entity48103 (0.03 or 0.1 mg/kg) lessened the elevation of blood @entity413 after @entity969 ingestion. The lower dose (0.03 mg/kg) retarded small intestinal absorption, but did not induce an influx of @entity969 into the cecum and large intestine, while the higher dose (0.1 mg/kg) caused an increased influx of @entity969 into the large bowel. These results indicated that @entity48103 retards the absorption of @entity1735 and reduces post-prandial @entity4854 .
