No abstract

The effects of cooking and chemical modification of purified starches on the relative rates and extent of their hydrolysis were studied in vitro by using purified human and rabbit pancreatic amylases. Comparison was made with an in vivo study of postprandial glucose and insulin response in adult rabbits. Uncooked starches showed negligible hydrolysis in vitro, whereas cooking (10 min, 100 degrees C) increased both the rate and extent of hydrolysis of all starches. Soluble potato starch was the most and potato amylose the least hydrolyzed. Unmodified tapioca and waxy corn starch were hydrolyzed at the same rate and to the same extent as soluble potato starches. In most cases chemical modification did not change the rate and extent of hydrolysis of the starches. Minor differences between human and rabbit pancreatic amylase exist, but there is a general resemblance between the two amylases in their starch-hydrolyzing properties (correlation coefficient = 0.90; P less than 0.001). The in vivo study showed that uncooked starches elicited no detectable glucose and insulin responses, whereas all the cooked starches except amylose caused glucose and insulin responses comparable to the response seen when feeding glucose. Chemically modified starches (especially waxy corn acetylated distarch adipate) seemed to promote a faster rate of absorption, but the total glucose response (i.e., for the entire 180-min duration) was similar for modified starches and their unmodified counter-parts. The in vivo results showed an overall qualitative similarity to the in vitro results but presented a quantitative difference in the magnitude of the responses for various starch preparations. A good correlation exists between the in vitro and in vivo results (correlation coefficient = 0.84; P less than 0.01). This indicates that the action of pancreatic amylases is an important determinant in the digestion and absorption of these carbohydrates.

Increases in AMP-18, pepsin and glandular stomach mass during normal postnatal development suggest that AMP-18 might be involved in gastric maturation, at least in the glandular portion. Dexamethasone induction of pepsin and AMP-18 and the subsequent increase in glandular stomach mass also suggest a possible role for AMP-18 in glandular stomach maturation. Dexamethasone apparently acts through the type II corticosteroid receptor to induce AMP-18.

No abstract