Published online Jun 7, 2014. doi: 10.3748/wjg.v20.i21.6534
Revised: December 5, 2013
Accepted: January 8, 2014
Published online: June 7, 2014
Processing time: 264 Days and 4.2 Hours
AIM: To describe the variation that divalent metal transporter 1 (DMT1) shows in patients after Roux-en-Y gastric bypass (RYGB) surgery.
METHODS: Prospective and analytical study of DMT1 level at the brush border of proximal jejunum in patients having undergone RYGB surgery. The mucosa of proximal jejunum forming the gastrojejunal anastomosis was biopsied during surgery and after 6 mo later with an endoscopic biopsy. All the patients received precise instructions regarding feeding and nutritional supplementation. Both samples were processed at the same time by immunohistochemistry and western blot. Samples were analysed by a pathologist. For statistical analysis, the χ2 and Wilcoxon tests were used.
RESULTS: Sixteen patients were recruited, 13 of whom completed the study. Twelve were women. Average age and body mass index (BMI) were 44.1 and 40.4, respectively. Both body weight and BMI decreased significantly during the study period, with an average percent excess weight loss (%EWL) of 60% ± 13.3% and an average percent excess BMI loss (%EBMIL) of 79.6% ± 21.6%. Only two patients presented with mild anaemia 6 mo after surgery, but their ferritin levels stayed within normal ranges. Staining for DMT1 showed a significant increase in the cytoplasm of enterocytes located at the tips of the villi (χ2 = 6.03; P = 0.049). Nevertheless, the total quantity of DMT1 decreased significantly (Z = 2.04; P = 0.04). Associated with these results, we observed a significant increase in goblet cells in the villi 6 mo postoperatively (Z = -2.47; P = 0.013).
CONCLUSION: Six months after RYGB surgery, patients exhibit an increase in DMT1 expression in the enterocytes of the tips of the villi at the proximal jejunum.
Core tip: Anaemia after Roux-en-Y gastric bypass surgery is one of the most common nutritional deficiencies. Different nutritional supplementation strategies have been developed to prevent this complication, but a subset of patients still develop it. This study brings readers the first report on the molecular changes that occur in the physiology of iron absorption in these patients.