AJP - Gastrointestinal and Liver Physiology, Vol 272, Issue 3 446-G453, Copyright © 1997 by American Physiological Society

ARTICLES

Dietary fructose enhances intestinal fructose transport and GLUT5 expression in weaning rats

R. Shu, E. S. David and R. P. Ferraris
Graduate School of Biomedical Sciences, University of Medicine and Dentistry of New Jersey, New Jersey Medical School, Newark 07103, USA.

Rates of fructose uptake by the small intestine of neonatal rats are typically very low from parturition through weaning but undergo a dramatic increase immediately after weaning is completed. In this study, we used intestinal fructose transport as a model to determine whether nutrient transport, normally enhanced only after completion of weaning, can be enhanced earlier during development. We found that ontogenetic changes in levels of GLUT5 mRNA correlate well with already known ontogenetic changes in rates of intestinal fructose transport: low levels and rates during suckling and weaning, and high levels and rates after weaning. In contrast, levels of GLUT2 and SGLT1 mRNA were relatively more elevated throughout the suckling and weaning periods. We then found that increased expression of GLUT5 mRNA caused by dietary fructose or sucrose paralleled diet-dependent increases in brush-border fructose uptake. Rates of brush-border glucose uptake and levels of SGLT1 and GLUT2 mRNA were not enhanced by dietary fructose, glucose, or sucrose. Finally, we found that rates of fructose uptake, levels of GLUT5 mRNA, and specific sucrase activity each increased with increasing concentrations of dietary fructose given precociously to midweaning rats. In contrast, brush-border glucose uptake was independent of dietary fructose concentration. Thus precocious introduction of dietary fructose causes enhanced expression of fructose transporters earlier during development. This effect is specific: only luminal fructose is effective, and only brush-border fructose transport can be modulated. These results unveil the potential for regulating nutrient transport early in development.

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