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Updated: Mar 9, 2026
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Roux-en-Y Gastric Bypass Operation in Rats
Published on: June 11, 2012
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Gastrointestinal Transcriptomic Response of Metabolic Vitamin B12 Pathways in Roux-en-Y Gastric Bypass
Priscila Sala1, Giliane Belarmino1, Raquel S Torrinhas1
1FMUSP-Department of Gastroenterology, Digestive Surgery Discipline, School of Medicine, University of São Paulo (LIM 35), São Paulo, Brazil.
Clinical and Translational Gastroenterology
|January 6, 2017
Summary
Roux-en-Y gastric bypass (RYGB) impacts vitamin B12 (B12) metabolism by altering gene expression in the gastrointestinal tract. Decreased transcobalamin I (TCN1) is a key factor in B12 deficiency post-RYGB.
Area of Science:
- Gastroenterology and Metabolic Surgery
- Molecular Biology
- Nutritional Science
Background:
- Vitamin B12 (B12) deficiency is common after Roux-en-Y gastric bypass (RYGB), potentially causing complications.
- Gastric fundus removal reduces intrinsic factor, but other B12 metabolism factors may be involved.
Purpose of the Study:
- To investigate changes in gastrointestinal (GI) gene expression related to B12 metabolism after RYGB.
- To identify genetic factors contributing to post-RYGB B12 deficiency.
Main Methods:
- Serial GI biopsies were collected from 20 obese women with type 2 diabetes before and 3 months after RYGB.
- Gene expression was analyzed using microarrays and validated with RT-qPCR.
Main Results:
- Significant changes in gene expression were observed for transcobalamin I (TCN1), gastric intrinsic factor (GIF), and cubilin (CUBN).
- TCN1 expression decreased in gastric remnant and excluded regions.
- CUBN expression increased in the duodenum, jejunum, and ileum, with jejunal changes validated by RT-qPCR.
Conclusions:
- RYGB alters multiple B12 pathway genes, contributing to postoperative B12 deficiency.
- Reduced TCN1 levels appear to be a primary cause of B12 deficiency.
- Increased CUBN suggests an adaptive response in intestinal tissue to compensate for impaired B12 absorption.
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