In newborn rodents, intestinal maturation involves delayed fructose transporter GLUT5 expression until weaning. In jejunoileal atresia (JIA), distal intestinal segments lack exposure to amniotic fluid-containing carbohydrates. We assessed in human newborns, the impact of intestinal maturation and obstruction on mucosal monosaccharide transporter expression.
Samples were obtained from 10 newborns operated for small intestinal atresia and from 17 adults undergoing gastroduodenoscopy and/or ileocolonoscopy. mRNA expression of the transporters SGLT1, GLUT1, GLUT2, GLUT5, and GLUT7 was measured in neonate samples proximal and distal of the atresia as well as in adult duodenum, ileum, and colon. Protein expression and localization was assessed using immunofluorescence.
Although mRNA expression of monosaccharide transporters did not significantly differ between newborn and adult samples, luminal fructose transporter GLUT5 protein was absent in 0- to 4-day-old neonates, but expressed in adults. The mRNA expression of the 5 tested monosaccharide transporters was unchanged distal from the JIA relative to proximal. Similarly, luminal sodium-dependent glucose transporter SGLT1 and basolateral GLUT2 were expressed proximal and distal to JIA as visualized by immunofluorescence staining. With the exception of glucose transporter GLUT1 that showed highest expression levels in colon, all investigated hexose transporters showed strongest expression in duodenum, lower levels in ileum and lowest in colon.
Human newborns lack small intestinal fructose transporter GLUT5 protein expression and small intestinal atresia does not affect the expression of hexose transporters.
*Institute of Physiology and Zurich Center for Integrative Human Physiology, University of Zurich (UZH), Zurich
†Department of Pediatric Surgery, University Children's Hospital Basel (UKBB), Basel, Switzerland.
Address correspondence and reprint requests to Raphael Nicolas Vuille-dit-Bille, MD, PhD, Institute of Physiology and Zurich Center for Integrative Human Physiology, Winterthurerstrasse 190, 8057 Zürich, Switzerland (e-mail: firstname.lastname@example.org).
Received 12 January, 2019
Accepted 2 May, 2019
The laboratory of F.V. is supported by Swiss National Science Foundation Grant 31_166430 and by the Swiss National Centre of Competence in Research Kidney Control of Homeostasis.
The authors report no conflicts of interest.
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