Regulation of Intestinal Fructose Transport in Neonatal Rats

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At birth, placental nutrition ceases and enteral nutrition begins. The small intestine abruptly acquires a new function: to absorb nutrients from milk. Shortly thereafter, the small intestine in weaning mammals faces a new challenge: to synthesize different types or different numbers of transporters to match expected changes in concentrations of different types of nutrients from the diet. How do intestinal cells make, and 'know' when to make, these transporters? Unlike other cells, intestinal cells are directly exposed to environmental signals present in the intestinal lumen. Hormones are known to regulate the appearance of intestinal enzymes, but their role in regulating intestinal nutrient transporters is not known. What is the importance of dietary or luminal signals relative to hormonal signals in modulating nutrient transporters? The long term objective of this project is to determine the mechanisms regulating intestinal nutrient transport during development. The intestinal fructose transporter GLUT5 is normally not made until after completion of weaning. However, precocious introduction of its substrate, dietary fructose, induces the early appearance of this transporter. GLUT5 will therefore be used as a model to evaluate the role of dietary and hormonal signals in modulating postnatal increases in intestinal nutrient transport. This project will attempt to identify nutrient-responsive regulatory mechanisms controlling gut development, and to reprogram normal developmental patterns of absorption in order to allow the intestine to process nutrients at an earlier stage of development. It will be important in furthering an understanding of mechanisms that control intestinal growth and maturation in premature infants. Fructose is an increasingly important component in American diets, and studies on intestinal fructose absorption per se, which have lagged way behind those on glucose and amino acid transport, have major nutritional significance.