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Background: Intestinal segments distal to congenital atresia have been suggested to be immature due to lack of luminal access of amniotic fluid (before birth) and nutrition (after birth). Whether the concomitant deficiency of luminal amino acids (AA) and glucose (Glc) has an impact on small intestinal amino acid- and glucose transporter expression, has never been tested.
Patients and methods: We therefore analyzed protein- (by immunoflurescence) and mRNA (by Real time RT-PCR) expression of several AA- and Glc transporters proximal and distal to small intestinal atresia in human newborns. To assess transporter function, we measured radiolabeled AA- and Glc uptake into small intestinal enterozytes located proximal and distal to the atretic segment. Furthermore villus morpholgy was analyzed by Hematoxylin-Eosin staining.
Results: Proximal sections showed morphological changes from normal intestinal architecture, consisting of villus atrophy and hemorrhages, necrotic areas and some lymphid aggregates within the lamina propria, whereas distal sections showed physiologic morphology. Preliminary results indicate a similar mRNA expression distal and proximal to small intestinal atresia for amino acid-, dipeptide-, monosaccharide- and fatty acid transporters, as well as for genes belonging to the Renin Angiotensin System (RAS). Protein expression of the amino acid transporter B⁰AT1 and its accessory RAS Protein Angiotensin Converting Enzyme 2 (ACE2), was similar in proximal- and distal segments. Radiolabeled uptake measurements showed a slight decrease in proximal sodium-independent Glucose- and Glutamine uptake, when compared to distal transport.
Conclusions: With respect to the genes and proteins tested, the absence of intestinal continuity in case of Small Intestinal Atresia seems not to affect epithelial gene and protein expression or function. This indicates amino acid- and monosaccharide transporter development independently of luminal components.