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Consumption of salt leads to ameliorate symptoms of metabolic disorder and change of gut microbiota
Purpose Metabolic diseases caused by high-carbohydrate and/or high-salt diets are becoming major public health concerns. However, the effects of salt on high-carbohydrate diet-induced obesity are unclear. Accordingly, in this study, we investigated the effects of high-salt intake on high-carbohydrat...
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Published in: | European journal of nutrition 2020-12, Vol.59 (8), p.3779-3790 |
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container_title | European journal of nutrition |
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creator | Do, Moon Ho Lee, Hye-Bin Oh, Mi-Jin Jhun, Hyunjhung Ha, Sang Keun Park, Ho-Young |
description | Purpose
Metabolic diseases caused by high-carbohydrate and/or high-salt diets are becoming major public health concerns. However, the effects of salt on high-carbohydrate diet-induced obesity are unclear. Accordingly, in this study, we investigated the effects of high-salt intake on high-carbohydrate diet-induced obesity.
Methods
We performed a 12-week study on gut microbiota and metabolic changes in high-rice diet (HRD) or HRD supplemented with high-salt (HRS)-fed C57BL/6 J mice by 16S rRNA analysis, glucose and insulin tolerance testing, gut barrier function, western blot and histological analysis. Moreover, the effects of salt on lipid metabolism were confirmed in vitro using 3T3-L1 cells.
Results
High salt intake decreased HRD-induced increases in body and white adipose tissue (WAT) weight. Alternatively, HRS did not reverse the observed increases in glucose intolerance and insulin resistance. Moreover, HRD caused changes in the gut microbiota, thereby impairing gut barrier function and increasing inflammation in the liver. HRS altered HRD-induced microbial composition, however, did not ameliorate gut barrier dysfunction or hepatic inflammation. HRS diets regulated the HRD-induced increase in peroxisome proliferator-activated receptor-γ (PPAR-γ) and lipid metabolism-related protein expression. Moreover, within WAT, HRS was found to reverse the observed decrease in adiponectin and increase in PPAR-γ expression induced by HRD. In vitro
,
high NaCl concentration also significantly reduced 3T3-L1 cell differentiation and modulated lipid metabolism without causing cytotoxicity.
Conclusion
These results indicate that high salt intake ameliorates metabolic changes associated with a high-rice diet, including changes in fecal microbiota composition. |
doi_str_mv | 10.1007/s00394-020-02209-0 |
format | article |
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Metabolic diseases caused by high-carbohydrate and/or high-salt diets are becoming major public health concerns. However, the effects of salt on high-carbohydrate diet-induced obesity are unclear. Accordingly, in this study, we investigated the effects of high-salt intake on high-carbohydrate diet-induced obesity.
Methods
We performed a 12-week study on gut microbiota and metabolic changes in high-rice diet (HRD) or HRD supplemented with high-salt (HRS)-fed C57BL/6 J mice by 16S rRNA analysis, glucose and insulin tolerance testing, gut barrier function, western blot and histological analysis. Moreover, the effects of salt on lipid metabolism were confirmed in vitro using 3T3-L1 cells.
Results
High salt intake decreased HRD-induced increases in body and white adipose tissue (WAT) weight. Alternatively, HRS did not reverse the observed increases in glucose intolerance and insulin resistance. Moreover, HRD caused changes in the gut microbiota, thereby impairing gut barrier function and increasing inflammation in the liver. HRS altered HRD-induced microbial composition, however, did not ameliorate gut barrier dysfunction or hepatic inflammation. HRS diets regulated the HRD-induced increase in peroxisome proliferator-activated receptor-γ (PPAR-γ) and lipid metabolism-related protein expression. Moreover, within WAT, HRS was found to reverse the observed decrease in adiponectin and increase in PPAR-γ expression induced by HRD. In vitro
,
high NaCl concentration also significantly reduced 3T3-L1 cell differentiation and modulated lipid metabolism without causing cytotoxicity.
Conclusion
These results indicate that high salt intake ameliorates metabolic changes associated with a high-rice diet, including changes in fecal microbiota composition.</description><identifier>ISSN: 1436-6207</identifier><identifier>EISSN: 1436-6215</identifier><identifier>DOI: 10.1007/s00394-020-02209-0</identifier><identifier>PMID: 32125529</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Adiponectin ; Adipose tissue ; Carbohydrates ; Cell differentiation ; Chemistry ; Chemistry and Materials Science ; Cytotoxicity ; Diet ; Fecal microflora ; Glucose tolerance ; High carbohydrate diet ; Insulin ; Intestinal microflora ; Intolerance ; Lipid metabolism ; Lipids ; Metabolic disorders ; Metabolism ; Microbiota ; Nutrition ; Obesity ; Original Contribution ; Peroxisome proliferator-activated receptors ; Protein turnover ; Public health ; rRNA 16S ; Salt ; Sodium chloride</subject><ispartof>European journal of nutrition, 2020-12, Vol.59 (8), p.3779-3790</ispartof><rights>Springer-Verlag GmbH Germany, part of Springer Nature 2020</rights><rights>Springer-Verlag GmbH Germany, part of Springer Nature 2020.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-2d90faf59c0f1f0f192b87065495381814314d77ff90528a1503618f3fd7e2a13</citedby><cites>FETCH-LOGICAL-c375t-2d90faf59c0f1f0f192b87065495381814314d77ff90528a1503618f3fd7e2a13</cites><orcidid>0000-0002-9966-9059</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32125529$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Do, Moon Ho</creatorcontrib><creatorcontrib>Lee, Hye-Bin</creatorcontrib><creatorcontrib>Oh, Mi-Jin</creatorcontrib><creatorcontrib>Jhun, Hyunjhung</creatorcontrib><creatorcontrib>Ha, Sang Keun</creatorcontrib><creatorcontrib>Park, Ho-Young</creatorcontrib><title>Consumption of salt leads to ameliorate symptoms of metabolic disorder and change of gut microbiota</title><title>European journal of nutrition</title><addtitle>Eur J Nutr</addtitle><addtitle>Eur J Nutr</addtitle><description>Purpose
Metabolic diseases caused by high-carbohydrate and/or high-salt diets are becoming major public health concerns. However, the effects of salt on high-carbohydrate diet-induced obesity are unclear. Accordingly, in this study, we investigated the effects of high-salt intake on high-carbohydrate diet-induced obesity.
Methods
We performed a 12-week study on gut microbiota and metabolic changes in high-rice diet (HRD) or HRD supplemented with high-salt (HRS)-fed C57BL/6 J mice by 16S rRNA analysis, glucose and insulin tolerance testing, gut barrier function, western blot and histological analysis. Moreover, the effects of salt on lipid metabolism were confirmed in vitro using 3T3-L1 cells.
Results
High salt intake decreased HRD-induced increases in body and white adipose tissue (WAT) weight. Alternatively, HRS did not reverse the observed increases in glucose intolerance and insulin resistance. Moreover, HRD caused changes in the gut microbiota, thereby impairing gut barrier function and increasing inflammation in the liver. HRS altered HRD-induced microbial composition, however, did not ameliorate gut barrier dysfunction or hepatic inflammation. HRS diets regulated the HRD-induced increase in peroxisome proliferator-activated receptor-γ (PPAR-γ) and lipid metabolism-related protein expression. Moreover, within WAT, HRS was found to reverse the observed decrease in adiponectin and increase in PPAR-γ expression induced by HRD. In vitro
,
high NaCl concentration also significantly reduced 3T3-L1 cell differentiation and modulated lipid metabolism without causing cytotoxicity.
Conclusion
These results indicate that high salt intake ameliorates metabolic changes associated with a high-rice diet, including changes in fecal microbiota composition.</description><subject>Adiponectin</subject><subject>Adipose tissue</subject><subject>Carbohydrates</subject><subject>Cell differentiation</subject><subject>Chemistry</subject><subject>Chemistry and Materials Science</subject><subject>Cytotoxicity</subject><subject>Diet</subject><subject>Fecal microflora</subject><subject>Glucose tolerance</subject><subject>High carbohydrate diet</subject><subject>Insulin</subject><subject>Intestinal microflora</subject><subject>Intolerance</subject><subject>Lipid metabolism</subject><subject>Lipids</subject><subject>Metabolic disorders</subject><subject>Metabolism</subject><subject>Microbiota</subject><subject>Nutrition</subject><subject>Obesity</subject><subject>Original Contribution</subject><subject>Peroxisome proliferator-activated receptors</subject><subject>Protein turnover</subject><subject>Public health</subject><subject>rRNA 16S</subject><subject>Salt</subject><subject>Sodium chloride</subject><issn>1436-6207</issn><issn>1436-6215</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><recordid>eNp9kT9PwzAQxS0EoqXwBRiQJRaWwNmO43hEFf-kSiwwW25il1RJXGxn6LfHoaVIDAwnW_Lv3vndQ-iSwC0BEHcBgMk8AwqpKMgMjtCU5KzICkr48eEOYoLOQlgDAGUFOUUTRgnlnMopquauD0O3iY3rsbM46Dbi1ug64Oiw7kzbOK-jwWGbINeFEepM1EvXNhWum-B8bTzWfY2rD92vzAishoi7pvJu2bioz9GJ1W0wF_tzht4fH97mz9ni9ellfr_IKiZ4zGgtwWrLZQWW2FSSLksBBc8lZyUpkxuS10JYK4HTUhMOyU1pma2FoZqwGbrZ6W68-xxMiKprQmXaVvfGDUFRJiD1CAEJvf6Drt3g-_Q7RXNBCs5lLhJFd1RyEoI3Vm1802m_VQTUGIHaRaBSBOo7AjVKX-2lh2Vn6kPLz84TwHZASE9pYf539j-yX7VYkDc</recordid><startdate>20201201</startdate><enddate>20201201</enddate><creator>Do, Moon Ho</creator><creator>Lee, Hye-Bin</creator><creator>Oh, Mi-Jin</creator><creator>Jhun, Hyunjhung</creator><creator>Ha, Sang Keun</creator><creator>Park, Ho-Young</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7RQ</scope><scope>7RV</scope><scope>7TS</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9-</scope><scope>K9.</scope><scope>KB0</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-9966-9059</orcidid></search><sort><creationdate>20201201</creationdate><title>Consumption of salt leads to ameliorate symptoms of metabolic disorder and change of gut microbiota</title><author>Do, Moon Ho ; Lee, Hye-Bin ; Oh, Mi-Jin ; Jhun, Hyunjhung ; Ha, Sang Keun ; Park, Ho-Young</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-2d90faf59c0f1f0f192b87065495381814314d77ff90528a1503618f3fd7e2a13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Adiponectin</topic><topic>Adipose tissue</topic><topic>Carbohydrates</topic><topic>Cell differentiation</topic><topic>Chemistry</topic><topic>Chemistry and Materials Science</topic><topic>Cytotoxicity</topic><topic>Diet</topic><topic>Fecal microflora</topic><topic>Glucose tolerance</topic><topic>High carbohydrate diet</topic><topic>Insulin</topic><topic>Intestinal microflora</topic><topic>Intolerance</topic><topic>Lipid metabolism</topic><topic>Lipids</topic><topic>Metabolic disorders</topic><topic>Metabolism</topic><topic>Microbiota</topic><topic>Nutrition</topic><topic>Obesity</topic><topic>Original Contribution</topic><topic>Peroxisome proliferator-activated receptors</topic><topic>Protein turnover</topic><topic>Public health</topic><topic>rRNA 16S</topic><topic>Salt</topic><topic>Sodium chloride</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Do, Moon Ho</creatorcontrib><creatorcontrib>Lee, Hye-Bin</creatorcontrib><creatorcontrib>Oh, Mi-Jin</creatorcontrib><creatorcontrib>Jhun, Hyunjhung</creatorcontrib><creatorcontrib>Ha, Sang Keun</creatorcontrib><creatorcontrib>Park, Ho-Young</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>ProQuest Career and Technical Education</collection><collection>Nursing & Allied Health Database</collection><collection>Physical Education Index</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Consumer Health Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>European journal of nutrition</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Do, Moon Ho</au><au>Lee, Hye-Bin</au><au>Oh, Mi-Jin</au><au>Jhun, Hyunjhung</au><au>Ha, Sang Keun</au><au>Park, Ho-Young</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Consumption of salt leads to ameliorate symptoms of metabolic disorder and change of gut microbiota</atitle><jtitle>European journal of nutrition</jtitle><stitle>Eur J Nutr</stitle><addtitle>Eur J Nutr</addtitle><date>2020-12-01</date><risdate>2020</risdate><volume>59</volume><issue>8</issue><spage>3779</spage><epage>3790</epage><pages>3779-3790</pages><issn>1436-6207</issn><eissn>1436-6215</eissn><abstract>Purpose
Metabolic diseases caused by high-carbohydrate and/or high-salt diets are becoming major public health concerns. However, the effects of salt on high-carbohydrate diet-induced obesity are unclear. Accordingly, in this study, we investigated the effects of high-salt intake on high-carbohydrate diet-induced obesity.
Methods
We performed a 12-week study on gut microbiota and metabolic changes in high-rice diet (HRD) or HRD supplemented with high-salt (HRS)-fed C57BL/6 J mice by 16S rRNA analysis, glucose and insulin tolerance testing, gut barrier function, western blot and histological analysis. Moreover, the effects of salt on lipid metabolism were confirmed in vitro using 3T3-L1 cells.
Results
High salt intake decreased HRD-induced increases in body and white adipose tissue (WAT) weight. Alternatively, HRS did not reverse the observed increases in glucose intolerance and insulin resistance. Moreover, HRD caused changes in the gut microbiota, thereby impairing gut barrier function and increasing inflammation in the liver. HRS altered HRD-induced microbial composition, however, did not ameliorate gut barrier dysfunction or hepatic inflammation. HRS diets regulated the HRD-induced increase in peroxisome proliferator-activated receptor-γ (PPAR-γ) and lipid metabolism-related protein expression. Moreover, within WAT, HRS was found to reverse the observed decrease in adiponectin and increase in PPAR-γ expression induced by HRD. In vitro
,
high NaCl concentration also significantly reduced 3T3-L1 cell differentiation and modulated lipid metabolism without causing cytotoxicity.
Conclusion
These results indicate that high salt intake ameliorates metabolic changes associated with a high-rice diet, including changes in fecal microbiota composition.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>32125529</pmid><doi>10.1007/s00394-020-02209-0</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0002-9966-9059</orcidid></addata></record> |
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subjects | Adiponectin Adipose tissue Carbohydrates Cell differentiation Chemistry Chemistry and Materials Science Cytotoxicity Diet Fecal microflora Glucose tolerance High carbohydrate diet Insulin Intestinal microflora Intolerance Lipid metabolism Lipids Metabolic disorders Metabolism Microbiota Nutrition Obesity Original Contribution Peroxisome proliferator-activated receptors Protein turnover Public health rRNA 16S Salt Sodium chloride |
title | Consumption of salt leads to ameliorate symptoms of metabolic disorder and change of gut microbiota |
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