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Mechanism of Roux-en-Y Gastric Bypass Treatment for Type 2 Diabetes in Rats

OBJECTIVES: Roux-en-Y gastric bypass (RYGB) is a novel therapy for diabetes. We aimed to explore the therapeutic mechanism of RYGB. METHODS: After RYGB, animal models were established, and gene expression profile of islets was assessed. Additionally, gastrointestinal hormones were measured using enz...

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Detalles Bibliográficos
Autores principales: Yu, Hongwei, Zheng, Xiyan, Zhang, Zongming
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer-Verlag 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3653054/
https://www.ncbi.nlm.nih.gov/pubmed/23580087
http://dx.doi.org/10.1007/s11605-013-2188-3
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author Yu, Hongwei
Zheng, Xiyan
Zhang, Zongming
author_facet Yu, Hongwei
Zheng, Xiyan
Zhang, Zongming
author_sort Yu, Hongwei
collection PubMed
description OBJECTIVES: Roux-en-Y gastric bypass (RYGB) is a novel therapy for diabetes. We aimed to explore the therapeutic mechanism of RYGB. METHODS: After RYGB, animal models were established, and gene expression profile of islets was assessed. Additionally, gastrointestinal hormones were measured using enzyme-linked immunosorbent assays. Ca(2+) was studied using confocal microscopy and patch-clamp technique. The morphology of islets and beta cells was observed using optical microscopy and electron microscopy. RESULTS: RYGB was an effective treatment in diabetic rats. Expression profiling data showed that RYGB produced a new metabolic environment and that gene expression changed to adapt to the new environment. The differential expression of genes associated with hormones, Ca(2+) and cellular proliferation was closely related to RYGB and diabetes metabolism. Furthermore, the data verified that RYGB led to changes in hormone level and enhanced Ca(2+) concentration changes and Ca(2+) channel activity. Morphological data showed that RYGB induced the proliferation of islets and improved the function of beta cells. CONCLUSIONS: RYGB promoted a new metabolic environment while triggering changes to adapt to the new environment. These changes promoted the cellular proliferation of islets and improved the function of beta cells. The quantity of beta cells increased, and their quality improved, ultimately leading to insulin secretion enhancement. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s11605-013-2188-3) contains supplementary material, which is available to authorized users.
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spelling pubmed-36530542013-05-16 Mechanism of Roux-en-Y Gastric Bypass Treatment for Type 2 Diabetes in Rats Yu, Hongwei Zheng, Xiyan Zhang, Zongming J Gastrointest Surg Original Article OBJECTIVES: Roux-en-Y gastric bypass (RYGB) is a novel therapy for diabetes. We aimed to explore the therapeutic mechanism of RYGB. METHODS: After RYGB, animal models were established, and gene expression profile of islets was assessed. Additionally, gastrointestinal hormones were measured using enzyme-linked immunosorbent assays. Ca(2+) was studied using confocal microscopy and patch-clamp technique. The morphology of islets and beta cells was observed using optical microscopy and electron microscopy. RESULTS: RYGB was an effective treatment in diabetic rats. Expression profiling data showed that RYGB produced a new metabolic environment and that gene expression changed to adapt to the new environment. The differential expression of genes associated with hormones, Ca(2+) and cellular proliferation was closely related to RYGB and diabetes metabolism. Furthermore, the data verified that RYGB led to changes in hormone level and enhanced Ca(2+) concentration changes and Ca(2+) channel activity. Morphological data showed that RYGB induced the proliferation of islets and improved the function of beta cells. CONCLUSIONS: RYGB promoted a new metabolic environment while triggering changes to adapt to the new environment. These changes promoted the cellular proliferation of islets and improved the function of beta cells. The quantity of beta cells increased, and their quality improved, ultimately leading to insulin secretion enhancement. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s11605-013-2188-3) contains supplementary material, which is available to authorized users. Springer-Verlag 2013-04-12 2013 /pmc/articles/PMC3653054/ /pubmed/23580087 http://dx.doi.org/10.1007/s11605-013-2188-3 Text en © The Author(s) 2013 https://creativecommons.org/licenses/by-nc/2.0/ Open Access This article is distributed under the terms of the Creative Commons Attribution License which permits any use, distribution, and reproduction in any medium, provided the original author(s) and the source are credited.
spellingShingle Original Article
Yu, Hongwei
Zheng, Xiyan
Zhang, Zongming
Mechanism of Roux-en-Y Gastric Bypass Treatment for Type 2 Diabetes in Rats
title Mechanism of Roux-en-Y Gastric Bypass Treatment for Type 2 Diabetes in Rats
title_full Mechanism of Roux-en-Y Gastric Bypass Treatment for Type 2 Diabetes in Rats
title_fullStr Mechanism of Roux-en-Y Gastric Bypass Treatment for Type 2 Diabetes in Rats
title_full_unstemmed Mechanism of Roux-en-Y Gastric Bypass Treatment for Type 2 Diabetes in Rats
title_short Mechanism of Roux-en-Y Gastric Bypass Treatment for Type 2 Diabetes in Rats
title_sort mechanism of roux-en-y gastric bypass treatment for type 2 diabetes in rats
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3653054/
https://www.ncbi.nlm.nih.gov/pubmed/23580087
http://dx.doi.org/10.1007/s11605-013-2188-3
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