The Buckwheat Iminosugar d‐Fagomine Attenuates Sucrose‐Induced Steatosis and Hypertension in Rats

Scope This study examines the long‐term functional effects of d‐fagomine on sucrose‐induced factors of metabolic dysfunctions and explores possible molecular mechanisms behind its action. Methods and results Wistar Kyoto rats are fed a 35% sucrose solution with d‐fagomine (or not, for comparison) or...

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Veröffentlicht in:Molecular nutrition & food research 2020-01, Vol.64 (1), p.e1900564-n/a
Hauptverfasser: Ramos‐Romero, Sara, Hereu, Mercè, Atienza, Lidia, Amézqueta, Susana, Casas, Josefina, Muñoz, Silvia, Medina, Isabel, Miralles‐Pérez, Bernat, Romeu, Marta, Torres, Josep L.
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container_start_page e1900564
container_title Molecular nutrition & food research
container_volume 64
creator Ramos‐Romero, Sara
Hereu, Mercè
Atienza, Lidia
Amézqueta, Susana
Casas, Josefina
Muñoz, Silvia
Medina, Isabel
Miralles‐Pérez, Bernat
Romeu, Marta
Torres, Josep L.
description Scope This study examines the long‐term functional effects of d‐fagomine on sucrose‐induced factors of metabolic dysfunctions and explores possible molecular mechanisms behind its action. Methods and results Wistar Kyoto rats are fed a 35% sucrose solution with d‐fagomine (or not, for comparison) or mineral water (controls) for 24 weeks. The following are recorded: body weight; energy intake; glucose tolerance; plasma leptin concentration and lipid profile; populations of Bacteroidetes, Firmicutes, bacteroidales, clostridiales, enterobacteriales, and Escherichia coli in feces; blood pressure; urine uric acid and F2t isoprostanes (F2‐IsoPs); perigonadal fat deposition; and hepatic histology and diacylglycerols (DAGs) in liver and adipose tissue. d‐Fagomine reduces sucrose‐induced hypertension, urine uric acid and F2‐IsoPs (markers of oxidative stress), steatosis, and liver DAGs, without significantly affecting perigonadal fat deposition, and impaired glucose tolerance. It also promotes excretion of enterobacteriales generated by the dietary intervention. Conclusion d‐fagomine counteracts sucrose‐induced steatosis and hypertension, presumably by reducing the postprandial levels of fructose in the liver. The buckwheat iminosugar d‐fagomine reduces high‐sucrose‐induced hypertension, urine uric acid, and F2‐isoprostanes (markers of oxidative stress), steatosis, and liver diacylglicerols, without affecting perigonadal fat deposition. It is suggested that d‐fagomine counteracts sucrose‐induced steatosis and hypertension by reducing the postprandial levels of fructose in the liver.
doi_str_mv 10.1002/mnfr.201900564
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Methods and results Wistar Kyoto rats are fed a 35% sucrose solution with d‐fagomine (or not, for comparison) or mineral water (controls) for 24 weeks. The following are recorded: body weight; energy intake; glucose tolerance; plasma leptin concentration and lipid profile; populations of Bacteroidetes, Firmicutes, bacteroidales, clostridiales, enterobacteriales, and Escherichia coli in feces; blood pressure; urine uric acid and F2t isoprostanes (F2‐IsoPs); perigonadal fat deposition; and hepatic histology and diacylglycerols (DAGs) in liver and adipose tissue. d‐Fagomine reduces sucrose‐induced hypertension, urine uric acid and F2‐IsoPs (markers of oxidative stress), steatosis, and liver DAGs, without significantly affecting perigonadal fat deposition, and impaired glucose tolerance. It also promotes excretion of enterobacteriales generated by the dietary intervention. Conclusion d‐fagomine counteracts sucrose‐induced steatosis and hypertension, presumably by reducing the postprandial levels of fructose in the liver. The buckwheat iminosugar d‐fagomine reduces high‐sucrose‐induced hypertension, urine uric acid, and F2‐isoprostanes (markers of oxidative stress), steatosis, and liver diacylglicerols, without affecting perigonadal fat deposition. It is suggested that d‐fagomine counteracts sucrose‐induced steatosis and hypertension by reducing the postprandial levels of fructose in the liver.</description><identifier>ISSN: 1613-4125</identifier><identifier>EISSN: 1613-4133</identifier><identifier>DOI: 10.1002/mnfr.201900564</identifier><identifier>PMID: 31657510</identifier><language>eng</language><publisher>Germany: Wiley Subscription Services, Inc</publisher><subject>Adipose tissue ; Adipose Tissue - drug effects ; Adipose Tissue - metabolism ; Animals ; Blood pressure ; Body weight ; Buckwheat ; Chemical compounds ; Deposition ; diabetes ; Diet ; Diglycerides - metabolism ; d‐fagomine ; E coli ; Energy intake ; Energy Intake - drug effects ; Fagopyrum - chemistry ; Fatty liver ; Fructose ; Gastrointestinal Microbiome - drug effects ; Glucose ; Glucose tolerance ; Histology ; Hypertension ; Hypertension - chemically induced ; Hypertension - drug therapy ; Imino Pyranoses - pharmacology ; Isoprostanes ; Isoprostanes - urine ; Leptin ; Leptin - blood ; Lipids ; Lipids - blood ; Liver ; Liver - drug effects ; Liver - metabolism ; Liver - pathology ; Male ; metabolic syndrome ; Mineral water ; Molecular modelling ; Non-alcoholic Fatty Liver Disease - chemically induced ; Non-alcoholic Fatty Liver Disease - drug therapy ; Oxidative stress ; Postprandial Period ; Rats, Inbred WKY ; Steatosis ; Sucrose ; Sucrose - toxicity ; Sugar ; Uric acid ; Uric Acid - blood ; Uric Acid - urine ; Urine</subject><ispartof>Molecular nutrition &amp; food research, 2020-01, Vol.64 (1), p.e1900564-n/a</ispartof><rights>2019 WILEY‐VCH Verlag GmbH &amp; Co. KGaA, Weinheim</rights><rights>2019 WILEY-VCH Verlag GmbH &amp; Co. KGaA, Weinheim.</rights><rights>2020 WILEY‐VCH Verlag GmbH &amp; Co. 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Methods and results Wistar Kyoto rats are fed a 35% sucrose solution with d‐fagomine (or not, for comparison) or mineral water (controls) for 24 weeks. The following are recorded: body weight; energy intake; glucose tolerance; plasma leptin concentration and lipid profile; populations of Bacteroidetes, Firmicutes, bacteroidales, clostridiales, enterobacteriales, and Escherichia coli in feces; blood pressure; urine uric acid and F2t isoprostanes (F2‐IsoPs); perigonadal fat deposition; and hepatic histology and diacylglycerols (DAGs) in liver and adipose tissue. d‐Fagomine reduces sucrose‐induced hypertension, urine uric acid and F2‐IsoPs (markers of oxidative stress), steatosis, and liver DAGs, without significantly affecting perigonadal fat deposition, and impaired glucose tolerance. It also promotes excretion of enterobacteriales generated by the dietary intervention. Conclusion d‐fagomine counteracts sucrose‐induced steatosis and hypertension, presumably by reducing the postprandial levels of fructose in the liver. The buckwheat iminosugar d‐fagomine reduces high‐sucrose‐induced hypertension, urine uric acid, and F2‐isoprostanes (markers of oxidative stress), steatosis, and liver diacylglicerols, without affecting perigonadal fat deposition. It is suggested that d‐fagomine counteracts sucrose‐induced steatosis and hypertension by reducing the postprandial levels of fructose in the liver.</description><subject>Adipose tissue</subject><subject>Adipose Tissue - drug effects</subject><subject>Adipose Tissue - metabolism</subject><subject>Animals</subject><subject>Blood pressure</subject><subject>Body weight</subject><subject>Buckwheat</subject><subject>Chemical compounds</subject><subject>Deposition</subject><subject>diabetes</subject><subject>Diet</subject><subject>Diglycerides - metabolism</subject><subject>d‐fagomine</subject><subject>E coli</subject><subject>Energy intake</subject><subject>Energy Intake - drug effects</subject><subject>Fagopyrum - chemistry</subject><subject>Fatty liver</subject><subject>Fructose</subject><subject>Gastrointestinal Microbiome - drug effects</subject><subject>Glucose</subject><subject>Glucose tolerance</subject><subject>Histology</subject><subject>Hypertension</subject><subject>Hypertension - chemically induced</subject><subject>Hypertension - drug therapy</subject><subject>Imino Pyranoses - pharmacology</subject><subject>Isoprostanes</subject><subject>Isoprostanes - urine</subject><subject>Leptin</subject><subject>Leptin - blood</subject><subject>Lipids</subject><subject>Lipids - blood</subject><subject>Liver</subject><subject>Liver - drug effects</subject><subject>Liver - metabolism</subject><subject>Liver - pathology</subject><subject>Male</subject><subject>metabolic syndrome</subject><subject>Mineral water</subject><subject>Molecular modelling</subject><subject>Non-alcoholic Fatty Liver Disease - chemically induced</subject><subject>Non-alcoholic Fatty Liver Disease - drug therapy</subject><subject>Oxidative stress</subject><subject>Postprandial Period</subject><subject>Rats, Inbred WKY</subject><subject>Steatosis</subject><subject>Sucrose</subject><subject>Sucrose - toxicity</subject><subject>Sugar</subject><subject>Uric acid</subject><subject>Uric Acid - blood</subject><subject>Uric Acid - urine</subject><subject>Urine</subject><issn>1613-4125</issn><issn>1613-4133</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkMFOAjEQhhujEUSvHk0Tz4udtrvdPSIRIUFNAM-b7raFRdjFdhvCzUfwGX0Sl4BcPc1k5vv_yfwI3QLpAiH0YV0a26UEEkLCiJ-hNkTAAg6MnZ96GrbQlXNLQhhQzi5Ri0EUihBIG-nZQuNHn39sF1rWeLQuysr5ubRY_Xx9D-S8aiYa9-pal17W2uGpz23ldLMdlcrnWuFp3UgrVzgsS4WHu422De2KqsRFiSeydtfowsiV0zfH2kHvg6dZfxiM355H_d44yLngPFAqE0AzHedCmFjFeRaLUIgsy8EolXBIDJXAecQhimVCuYhlDMTIMA9DIwXroPuD78ZWn167Ol1W3pbNyZQyBgKAUtJQ3QO1f8RZbdKNLdbS7lIg6T7VdJ9qekq1EdwdbX221uqE_8XYAPwAbIuV3v1jl768DiYsYpz9App6hZY</recordid><startdate>202001</startdate><enddate>202001</enddate><creator>Ramos‐Romero, Sara</creator><creator>Hereu, Mercè</creator><creator>Atienza, Lidia</creator><creator>Amézqueta, Susana</creator><creator>Casas, Josefina</creator><creator>Muñoz, Silvia</creator><creator>Medina, Isabel</creator><creator>Miralles‐Pérez, Bernat</creator><creator>Romeu, Marta</creator><creator>Torres, Josep L.</creator><general>Wiley Subscription Services, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QO</scope><scope>7QP</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><orcidid>https://orcid.org/0000-0002-9293-4454</orcidid></search><sort><creationdate>202001</creationdate><title>The Buckwheat Iminosugar d‐Fagomine Attenuates Sucrose‐Induced Steatosis and Hypertension in Rats</title><author>Ramos‐Romero, Sara ; Hereu, Mercè ; Atienza, Lidia ; Amézqueta, Susana ; Casas, Josefina ; Muñoz, Silvia ; Medina, Isabel ; Miralles‐Pérez, Bernat ; Romeu, Marta ; Torres, Josep L.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4744-ddb712be8c77f8d8cb87577bbc1fdd9419f2a14464168a92478a810fa5c55fa73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Adipose tissue</topic><topic>Adipose Tissue - drug effects</topic><topic>Adipose Tissue - metabolism</topic><topic>Animals</topic><topic>Blood pressure</topic><topic>Body weight</topic><topic>Buckwheat</topic><topic>Chemical compounds</topic><topic>Deposition</topic><topic>diabetes</topic><topic>Diet</topic><topic>Diglycerides - metabolism</topic><topic>d‐fagomine</topic><topic>E coli</topic><topic>Energy intake</topic><topic>Energy Intake - drug effects</topic><topic>Fagopyrum - chemistry</topic><topic>Fatty liver</topic><topic>Fructose</topic><topic>Gastrointestinal Microbiome - drug effects</topic><topic>Glucose</topic><topic>Glucose tolerance</topic><topic>Histology</topic><topic>Hypertension</topic><topic>Hypertension - chemically induced</topic><topic>Hypertension - drug therapy</topic><topic>Imino Pyranoses - pharmacology</topic><topic>Isoprostanes</topic><topic>Isoprostanes - urine</topic><topic>Leptin</topic><topic>Leptin - blood</topic><topic>Lipids</topic><topic>Lipids - blood</topic><topic>Liver</topic><topic>Liver - drug effects</topic><topic>Liver - metabolism</topic><topic>Liver - pathology</topic><topic>Male</topic><topic>metabolic syndrome</topic><topic>Mineral water</topic><topic>Molecular modelling</topic><topic>Non-alcoholic Fatty Liver Disease - chemically induced</topic><topic>Non-alcoholic Fatty Liver Disease - drug therapy</topic><topic>Oxidative stress</topic><topic>Postprandial Period</topic><topic>Rats, Inbred WKY</topic><topic>Steatosis</topic><topic>Sucrose</topic><topic>Sucrose - toxicity</topic><topic>Sugar</topic><topic>Uric acid</topic><topic>Uric Acid - blood</topic><topic>Uric Acid - urine</topic><topic>Urine</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ramos‐Romero, Sara</creatorcontrib><creatorcontrib>Hereu, Mercè</creatorcontrib><creatorcontrib>Atienza, Lidia</creatorcontrib><creatorcontrib>Amézqueta, Susana</creatorcontrib><creatorcontrib>Casas, Josefina</creatorcontrib><creatorcontrib>Muñoz, Silvia</creatorcontrib><creatorcontrib>Medina, Isabel</creatorcontrib><creatorcontrib>Miralles‐Pérez, Bernat</creatorcontrib><creatorcontrib>Romeu, Marta</creatorcontrib><creatorcontrib>Torres, Josep L.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Calcium &amp; Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><jtitle>Molecular nutrition &amp; food research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ramos‐Romero, Sara</au><au>Hereu, Mercè</au><au>Atienza, Lidia</au><au>Amézqueta, Susana</au><au>Casas, Josefina</au><au>Muñoz, Silvia</au><au>Medina, Isabel</au><au>Miralles‐Pérez, Bernat</au><au>Romeu, Marta</au><au>Torres, Josep L.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Buckwheat Iminosugar d‐Fagomine Attenuates Sucrose‐Induced Steatosis and Hypertension in Rats</atitle><jtitle>Molecular nutrition &amp; food research</jtitle><addtitle>Mol Nutr Food Res</addtitle><date>2020-01</date><risdate>2020</risdate><volume>64</volume><issue>1</issue><spage>e1900564</spage><epage>n/a</epage><pages>e1900564-n/a</pages><issn>1613-4125</issn><eissn>1613-4133</eissn><abstract>Scope This study examines the long‐term functional effects of d‐fagomine on sucrose‐induced factors of metabolic dysfunctions and explores possible molecular mechanisms behind its action. Methods and results Wistar Kyoto rats are fed a 35% sucrose solution with d‐fagomine (or not, for comparison) or mineral water (controls) for 24 weeks. The following are recorded: body weight; energy intake; glucose tolerance; plasma leptin concentration and lipid profile; populations of Bacteroidetes, Firmicutes, bacteroidales, clostridiales, enterobacteriales, and Escherichia coli in feces; blood pressure; urine uric acid and F2t isoprostanes (F2‐IsoPs); perigonadal fat deposition; and hepatic histology and diacylglycerols (DAGs) in liver and adipose tissue. d‐Fagomine reduces sucrose‐induced hypertension, urine uric acid and F2‐IsoPs (markers of oxidative stress), steatosis, and liver DAGs, without significantly affecting perigonadal fat deposition, and impaired glucose tolerance. It also promotes excretion of enterobacteriales generated by the dietary intervention. Conclusion d‐fagomine counteracts sucrose‐induced steatosis and hypertension, presumably by reducing the postprandial levels of fructose in the liver. The buckwheat iminosugar d‐fagomine reduces high‐sucrose‐induced hypertension, urine uric acid, and F2‐isoprostanes (markers of oxidative stress), steatosis, and liver diacylglicerols, without affecting perigonadal fat deposition. It is suggested that d‐fagomine counteracts sucrose‐induced steatosis and hypertension by reducing the postprandial levels of fructose in the liver.</abstract><cop>Germany</cop><pub>Wiley Subscription Services, Inc</pub><pmid>31657510</pmid><doi>10.1002/mnfr.201900564</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0002-9293-4454</orcidid><oa>free_for_read</oa></addata></record>
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subjects Adipose tissue
Adipose Tissue - drug effects
Adipose Tissue - metabolism
Animals
Blood pressure
Body weight
Buckwheat
Chemical compounds
Deposition
diabetes
Diet
Diglycerides - metabolism
d‐fagomine
E coli
Energy intake
Energy Intake - drug effects
Fagopyrum - chemistry
Fatty liver
Fructose
Gastrointestinal Microbiome - drug effects
Glucose
Glucose tolerance
Histology
Hypertension
Hypertension - chemically induced
Hypertension - drug therapy
Imino Pyranoses - pharmacology
Isoprostanes
Isoprostanes - urine
Leptin
Leptin - blood
Lipids
Lipids - blood
Liver
Liver - drug effects
Liver - metabolism
Liver - pathology
Male
metabolic syndrome
Mineral water
Molecular modelling
Non-alcoholic Fatty Liver Disease - chemically induced
Non-alcoholic Fatty Liver Disease - drug therapy
Oxidative stress
Postprandial Period
Rats, Inbred WKY
Steatosis
Sucrose
Sucrose - toxicity
Sugar
Uric acid
Uric Acid - blood
Uric Acid - urine
Urine
title The Buckwheat Iminosugar d‐Fagomine Attenuates Sucrose‐Induced Steatosis and Hypertension in Rats
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