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Roux-en-Y Gastric Bypass Improved Insulin Resistance via Alteration of the Human Gut Microbiome and Alleviation of Endotoxemia
Background. Obesity is a main contributing factor for the development of glucose intolerance and type 2 diabetes mellitus (T2D). Roux-en-Y gastric bypass (RYGB) is believed to be one of the most effective treatments to reduce body weight and improve glucose metabolism. In this study, we sought to ex...
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description | Background. Obesity is a main contributing factor for the development of glucose intolerance and type 2 diabetes mellitus (T2D). Roux-en-Y gastric bypass (RYGB) is believed to be one of the most effective treatments to reduce body weight and improve glucose metabolism. In this study, we sought to explore the underlying mechanisms of weight reduction and insulin resistance improvement after RYGB. Methods. This was a prospective observational study using consecutive samples of 14 obese subjects undergoing bariatric surgery. Main assessments were serum indexes (blood metabolites, glucose-lipid regulating hormones, trimethylamine-N-oxide (TMAO), and lipopolysaccharide-binding protein (LBP), fecal short-chain fatty acids (SCFAs), and gut microbiota. Correlation analysis of the factors changed by RYGB was used to indicate the potential mechanism by which surgery improves insulin resistance. Results. The subjects showed significant improvement on indices of obesity and insulin resistance and a correlated change of gut microbiota components at 1 month, 3 months, and 6 months post-RYGB operation. In particular, the abundance of a counterobese strain, Akkemansia muciniphila, had gradually increased with the postoperative time. Moreover, these changes were negatively correlated to serum levels of LBP and positively correlated to serum TMAO and fecal SCFAs. Conclusions. Our findings uncovered links between intestinal microbiota alterations, circulating endotoxemia, and insulin resistance. This suggests that the underlying mechanism of protection of the intestine by RYGB in obesity may be through changing the gut microbiota. |
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Obesity is a main contributing factor for the development of glucose intolerance and type 2 diabetes mellitus (T2D). Roux-en-Y gastric bypass (RYGB) is believed to be one of the most effective treatments to reduce body weight and improve glucose metabolism. In this study, we sought to explore the underlying mechanisms of weight reduction and insulin resistance improvement after RYGB. Methods. This was a prospective observational study using consecutive samples of 14 obese subjects undergoing bariatric surgery. Main assessments were serum indexes (blood metabolites, glucose-lipid regulating hormones, trimethylamine-N-oxide (TMAO), and lipopolysaccharide-binding protein (LBP), fecal short-chain fatty acids (SCFAs), and gut microbiota. Correlation analysis of the factors changed by RYGB was used to indicate the potential mechanism by which surgery improves insulin resistance. Results. The subjects showed significant improvement on indices of obesity and insulin resistance and a correlated change of gut microbiota components at 1 month, 3 months, and 6 months post-RYGB operation. In particular, the abundance of a counterobese strain, Akkemansia muciniphila, had gradually increased with the postoperative time. Moreover, these changes were negatively correlated to serum levels of LBP and positively correlated to serum TMAO and fecal SCFAs. Conclusions. Our findings uncovered links between intestinal microbiota alterations, circulating endotoxemia, and insulin resistance. This suggests that the underlying mechanism of protection of the intestine by RYGB in obesity may be through changing the gut microbiota.</description><identifier>ISSN: 2314-6133</identifier><identifier>EISSN: 2314-6141</identifier><identifier>DOI: 10.1155/2021/5554991</identifier><identifier>PMID: 34337024</identifier><language>eng</language><publisher>New York: Hindawi</publisher><subject>Analysis ; Body weight ; Care and treatment ; Correlation analysis ; Diabetes mellitus ; Diabetes mellitus (non-insulin dependent) ; Digestive system ; Endotoxemia ; Fatty acids ; Gastric bypass ; Gastrointestinal surgery ; Gastrointestinal tract ; Glucose ; Glucose metabolism ; Glucose tolerance ; Health aspects ; Hormones ; Insulin ; Insulin resistance ; Intestinal microflora ; Intestine ; Intolerance ; Lipids ; Lipopolysaccharide-binding protein ; Lipopolysaccharides ; Metabolites ; Methods ; Microbiomes ; Microbiota ; Microbiota (Symbiotic organisms) ; Obesity ; Patient outcomes ; Prognosis ; Risk factors ; Serum levels ; Surgery ; Testing ; Trimethylamine ; Trimethylamine-N-oxide ; Weight reduction</subject><ispartof>BioMed research international, 2021, Vol.2021, p.1-14</ispartof><rights>Copyright © 2021 Qiping Shi et al.</rights><rights>COPYRIGHT 2021 John Wiley & Sons, Inc.</rights><rights>Copyright © 2021 Qiping Shi et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. https://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2021 Qiping Shi et al. 2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c481t-19a80f540e863524b859d11d54a0b242b867044278995680bdfe4345b4abc6bb3</citedby><cites>FETCH-LOGICAL-c481t-19a80f540e863524b859d11d54a0b242b867044278995680bdfe4345b4abc6bb3</cites><orcidid>0000-0002-6418-1985 ; 0000-0001-6524-8777 ; 0000-0003-2576-7462</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2554894951/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2554894951?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,780,784,885,4024,25753,27923,27924,27925,37012,37013,44590,75126</link.rule.ids></links><search><contributor>Wang, Bing</contributor><contributor>Bing Wang</contributor><creatorcontrib>Shi, Qiping</creatorcontrib><creatorcontrib>Wang, Qian</creatorcontrib><creatorcontrib>Zhong, Hui</creatorcontrib><creatorcontrib>Li, Dehai</creatorcontrib><creatorcontrib>Yu, Shuxing</creatorcontrib><creatorcontrib>Yang, Hengwen</creatorcontrib><creatorcontrib>Wang, Cunchuan</creatorcontrib><creatorcontrib>Yin, Zhinan</creatorcontrib><title>Roux-en-Y Gastric Bypass Improved Insulin Resistance via Alteration of the Human Gut Microbiome and Alleviation of Endotoxemia</title><title>BioMed research international</title><description>Background. Obesity is a main contributing factor for the development of glucose intolerance and type 2 diabetes mellitus (T2D). Roux-en-Y gastric bypass (RYGB) is believed to be one of the most effective treatments to reduce body weight and improve glucose metabolism. In this study, we sought to explore the underlying mechanisms of weight reduction and insulin resistance improvement after RYGB. Methods. This was a prospective observational study using consecutive samples of 14 obese subjects undergoing bariatric surgery. Main assessments were serum indexes (blood metabolites, glucose-lipid regulating hormones, trimethylamine-N-oxide (TMAO), and lipopolysaccharide-binding protein (LBP), fecal short-chain fatty acids (SCFAs), and gut microbiota. Correlation analysis of the factors changed by RYGB was used to indicate the potential mechanism by which surgery improves insulin resistance. Results. The subjects showed significant improvement on indices of obesity and insulin resistance and a correlated change of gut microbiota components at 1 month, 3 months, and 6 months post-RYGB operation. In particular, the abundance of a counterobese strain, Akkemansia muciniphila, had gradually increased with the postoperative time. Moreover, these changes were negatively correlated to serum levels of LBP and positively correlated to serum TMAO and fecal SCFAs. Conclusions. Our findings uncovered links between intestinal microbiota alterations, circulating endotoxemia, and insulin resistance. This suggests that the underlying mechanism of protection of the intestine by RYGB in obesity may be through changing the gut microbiota.</description><subject>Analysis</subject><subject>Body weight</subject><subject>Care and treatment</subject><subject>Correlation analysis</subject><subject>Diabetes mellitus</subject><subject>Diabetes mellitus (non-insulin dependent)</subject><subject>Digestive system</subject><subject>Endotoxemia</subject><subject>Fatty acids</subject><subject>Gastric bypass</subject><subject>Gastrointestinal surgery</subject><subject>Gastrointestinal tract</subject><subject>Glucose</subject><subject>Glucose metabolism</subject><subject>Glucose tolerance</subject><subject>Health aspects</subject><subject>Hormones</subject><subject>Insulin</subject><subject>Insulin resistance</subject><subject>Intestinal microflora</subject><subject>Intestine</subject><subject>Intolerance</subject><subject>Lipids</subject><subject>Lipopolysaccharide-binding protein</subject><subject>Lipopolysaccharides</subject><subject>Metabolites</subject><subject>Methods</subject><subject>Microbiomes</subject><subject>Microbiota</subject><subject>Microbiota (Symbiotic organisms)</subject><subject>Obesity</subject><subject>Patient outcomes</subject><subject>Prognosis</subject><subject>Risk factors</subject><subject>Serum levels</subject><subject>Surgery</subject><subject>Testing</subject><subject>Trimethylamine</subject><subject>Trimethylamine-N-oxide</subject><subject>Weight reduction</subject><issn>2314-6133</issn><issn>2314-6141</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><recordid>eNp90s9rFDEUB_BBFFtqb_4BAS-Cjs2Pl5nkImxL3S5UhKIHTyGZyXRTZpI1yaztxb_dLLtW9NBcEsgn38cLr6peE_yBEM7PKKbkjHMOUpJn1TFlBOqGAHn-eGbsqDpN6Q6XJUiDZfOyOmLAWIspHFe_bsJ8X1tff0dLnXJ0HTp_2OiU0GraxLC1PVr5NI_OoxubXMradxZtnUaLMduoswsehQHltUVX86Q9Ws4ZfXZdDMaFySLt-0JHW578sZe-Dznc28npV9WLQY_Jnh72k-rbp8uvF1f19Zfl6mJxXXcgSK6J1AIPHLAVDeMUjOCyJ6TnoLGhQI1oWgxAWyElbwQ2_WCBATegTdcYw06qj_vczWwm23fW56hHtYlu0vFBBe3UvzferdVt2CpBJWDaloC3h4AYfsw2ZTW51Nlx1N6GOSnKecuBSM4KffMfvQtz9KW9nQIhQXLyV93q0Srnh1DqdrtQtWhkIwShvH1aCcYFlhiKer9X5ddTinZ4bIxgtZsTtZsTdZiTwt_t-dr5Xv90T-vfFTe4xg</recordid><startdate>2021</startdate><enddate>2021</enddate><creator>Shi, Qiping</creator><creator>Wang, Qian</creator><creator>Zhong, Hui</creator><creator>Li, Dehai</creator><creator>Yu, Shuxing</creator><creator>Yang, 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Gastric Bypass Improved Insulin Resistance via Alteration of the Human Gut Microbiome and Alleviation of Endotoxemia</title><author>Shi, Qiping ; Wang, Qian ; Zhong, Hui ; Li, Dehai ; Yu, Shuxing ; Yang, Hengwen ; Wang, Cunchuan ; Yin, Zhinan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c481t-19a80f540e863524b859d11d54a0b242b867044278995680bdfe4345b4abc6bb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Analysis</topic><topic>Body weight</topic><topic>Care and treatment</topic><topic>Correlation analysis</topic><topic>Diabetes mellitus</topic><topic>Diabetes mellitus (non-insulin dependent)</topic><topic>Digestive system</topic><topic>Endotoxemia</topic><topic>Fatty acids</topic><topic>Gastric bypass</topic><topic>Gastrointestinal surgery</topic><topic>Gastrointestinal tract</topic><topic>Glucose</topic><topic>Glucose metabolism</topic><topic>Glucose tolerance</topic><topic>Health aspects</topic><topic>Hormones</topic><topic>Insulin</topic><topic>Insulin resistance</topic><topic>Intestinal microflora</topic><topic>Intestine</topic><topic>Intolerance</topic><topic>Lipids</topic><topic>Lipopolysaccharide-binding protein</topic><topic>Lipopolysaccharides</topic><topic>Metabolites</topic><topic>Methods</topic><topic>Microbiomes</topic><topic>Microbiota</topic><topic>Microbiota (Symbiotic organisms)</topic><topic>Obesity</topic><topic>Patient outcomes</topic><topic>Prognosis</topic><topic>Risk factors</topic><topic>Serum levels</topic><topic>Surgery</topic><topic>Testing</topic><topic>Trimethylamine</topic><topic>Trimethylamine-N-oxide</topic><topic>Weight reduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shi, Qiping</creatorcontrib><creatorcontrib>Wang, Qian</creatorcontrib><creatorcontrib>Zhong, Hui</creatorcontrib><creatorcontrib>Li, Dehai</creatorcontrib><creatorcontrib>Yu, 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international</jtitle><date>2021</date><risdate>2021</risdate><volume>2021</volume><spage>1</spage><epage>14</epage><pages>1-14</pages><issn>2314-6133</issn><eissn>2314-6141</eissn><abstract>Background. Obesity is a main contributing factor for the development of glucose intolerance and type 2 diabetes mellitus (T2D). Roux-en-Y gastric bypass (RYGB) is believed to be one of the most effective treatments to reduce body weight and improve glucose metabolism. In this study, we sought to explore the underlying mechanisms of weight reduction and insulin resistance improvement after RYGB. Methods. This was a prospective observational study using consecutive samples of 14 obese subjects undergoing bariatric surgery. Main assessments were serum indexes (blood metabolites, glucose-lipid regulating hormones, trimethylamine-N-oxide (TMAO), and lipopolysaccharide-binding protein (LBP), fecal short-chain fatty acids (SCFAs), and gut microbiota. Correlation analysis of the factors changed by RYGB was used to indicate the potential mechanism by which surgery improves insulin resistance. Results. The subjects showed significant improvement on indices of obesity and insulin resistance and a correlated change of gut microbiota components at 1 month, 3 months, and 6 months post-RYGB operation. In particular, the abundance of a counterobese strain, Akkemansia muciniphila, had gradually increased with the postoperative time. Moreover, these changes were negatively correlated to serum levels of LBP and positively correlated to serum TMAO and fecal SCFAs. Conclusions. Our findings uncovered links between intestinal microbiota alterations, circulating endotoxemia, and insulin resistance. This suggests that the underlying mechanism of protection of the intestine by RYGB in obesity may be through changing the gut microbiota.</abstract><cop>New York</cop><pub>Hindawi</pub><pmid>34337024</pmid><doi>10.1155/2021/5554991</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0002-6418-1985</orcidid><orcidid>https://orcid.org/0000-0001-6524-8777</orcidid><orcidid>https://orcid.org/0000-0003-2576-7462</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Analysis Body weight Care and treatment Correlation analysis Diabetes mellitus Diabetes mellitus (non-insulin dependent) Digestive system Endotoxemia Fatty acids Gastric bypass Gastrointestinal surgery Gastrointestinal tract Glucose Glucose metabolism Glucose tolerance Health aspects Hormones Insulin Insulin resistance Intestinal microflora Intestine Intolerance Lipids Lipopolysaccharide-binding protein Lipopolysaccharides Metabolites Methods Microbiomes Microbiota Microbiota (Symbiotic organisms) Obesity Patient outcomes Prognosis Risk factors Serum levels Surgery Testing Trimethylamine Trimethylamine-N-oxide Weight reduction |
title | Roux-en-Y Gastric Bypass Improved Insulin Resistance via Alteration of the Human Gut Microbiome and Alleviation of Endotoxemia |
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