Abstract 1686 Poster Session I, Saturday, 5/1 (poster 120)

Starches are the most common carbohydrates in the postweaning human diet. Salivary and pancreatic amylase secretion and activity are low until 3-4 months of age, so the feeding of cereals to young infants is not recommended. Nevertheless, such feeding frequently occurs and results in efficient absorption and utilization of dietary starches. Furthermore, glucose oligomers (Polycoseâ„¢) are commonly fed to young infants, including prematures. Brush border maltase-glucoamylase complex (MGA), which splits glucose from linear starch and oligosaccharides, may provide an alternate pathway for starch digestion, compensating for the physiological immaturity of amylase. In mice, MGA is low at birth but increases upon weaning, and feeding weaned animals a high-starch diet rapidly increases MGA activity. We tested the hypothesis that feeding immature mice a diet high in glucose oligomers precociously induces MGA. Groups of four or more 6- to 8-day-old mice received percutaneous gastrostomies and were raised using the "pup in a cup" model, exclusively fed artificial formulas, for one week. One formula, a mouse milk substitute, had a relative macronutrient composition identical to mouse milk, with 4% of calories from lactose. A second formula had 20% of calories from Polycose and was normal in protein and low in fat. Weight gain of artificially reared pups approximated that of mother-fed pups, which served as controls. Measurements included assays of jejunal MGA (glucoamylase, oligosaccharidase, and maltase activities) by the Dahlqvist method and oxidation of 13-C labeled starch or glucose to 13-CO2 in breath. Amylase is not detected in these assays. Differences in MGA activities among the groups did not attain statistical significance. The magnitude of oxidation of a starch load to CO2 was not different among the three groups. Oxidation of starch was equivalent to oxidation of glucose in suckling pups. However, pups fed formula containing glucose oligomers demonstrated 1.5- to 2.6-fold greater oxidation of a glucose load to CO2 compared to a starch load (p<0.02). We conclude that feeding a diet containing 20% of calories from glucose oligomers for one week to mouse pups does not precociously induce MGA and has no effect on capacity for starch oxidation, despite enhanced glucose utilization. We therefore conclude that starch hydrolysis, catalyzed by MGA, is rate-limiting for starch oxidation during development. Colonic salvage may be an important mechanism for starch digestion in pups fed glucose oligomers. The mechanism underlying enhanced glucose oxidation in response to the high-carbohydrate diet is under investigation. We anticipate that the paradigm of the artificially reared mouse will be useful in the study of nutrient-gene interactions during development in transgenic and knockout mice.