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1 Department of Pediatrics, David Geffen School of Medicine at University of California Los Angeles, Mattel Children's Hospital, Los Angeles, California 90095-1752; 2 Department of Pediatrics, the University of Arizona College of Medicine, Steele Memorial Children's Research Center, and 3 Department of Microbiology and Immunology, the University of Arizona College of Medicine, Tucson, Arizona 85724-5073; and 4 Department of Pediatrics, University of California at Davis, Sacramento, California, 95817
Milk-borne insulin-like growth factors (IGFs) enhance nutrient absorption in the immature intestine, which is characterized by low levels of glucose oxidation. We therefore hypothesized that feeding a rat milk substitute (RMS) devoid of growth factors to rat pups would lower serum glucose levels relative to dam-fed control rats and that supplementation of RMS with physiological doses of either IGF-I or IGF-II would normalize serum glucose levels via increased jejunal glucose transporter 2 (GLUT2) and high-affinity Na+-glucose cotransporter (SGLT1) expression. We found lower serum glucose concentrations in RMS-fed pups; in contrast, serum glucose levels in the IGF-supplemented pups were similar to those of dam-fed controls. RT-PCR and laser scanning confocal microscopy similarly demonstrated that IGF supplementation increased expression of jejunal glucose transporters. Further experiments demonstrated that IGF supplementation altered mRNA levels of key mitochondrial enzymes without altering jejunal lactase activity. We conclude that IGF-I and IGF-II supplementation increases serum glucose levels in the immature rat pup fed artificial formula and alters gene expression of the jejunal glucose transporters.
SGLT1; GLUT2; GLUT1; fatty acid oxidation; glucose oxidation
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