A study on molecular mechanisms of adiposis induced by long-term treatment of high-fat and high-sucrose in C57BL/6J mice
Adiposis is reputed as a twin disease of type 2 diabetes and greatly harmful to human health. In order to understand the molecular mechanisms of adiposis, the changes of physiological, pathological, epigenetic and correlative gene expression were investigated during the adiposis development of C57BL...
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| Veröffentlicht in: | Physiological research 2019-01, Vol.68 (1), p.75-87 |
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| creator | Li, X Tu, P Umar, M Liu, Q Luo, W Yang, X Zhu, J Kong, D Li, M |
| description | Adiposis is reputed as a twin disease of type 2 diabetes and greatly harmful to human health. In order to understand the molecular mechanisms of adiposis, the changes of physiological, pathological, epigenetic and correlative gene expression were investigated during the adiposis development of C57BL/6J mice induced by long time (9 months) high-fat and high-sucrose diet (HFSD) sustainably. The results showed that mRNA transcription level of the Leptin, Glut4 and Glut2 genes have been obviously changed, which exhibit a negative correlation with methylation on their promoter DNA. The results also revealed that HFSD induced higher level of DNA methyltransferase 1 (DNMT1) in fat tissue might play important role in regulating the changes of methylation pattern on Glut4 and Leptin genes, and which might be one of the molecular mechanisms for the adiposis development. |
| doi_str_mv | 10.33549/physiolres.933830 |
| format | Article |
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In order to understand the molecular mechanisms of adiposis, the changes of physiological, pathological, epigenetic and correlative gene expression were investigated during the adiposis development of C57BL/6J mice induced by long time (9 months) high-fat and high-sucrose diet (HFSD) sustainably. The results showed that mRNA transcription level of the Leptin, Glut4 and Glut2 genes have been obviously changed, which exhibit a negative correlation with methylation on their promoter DNA. The results also revealed that HFSD induced higher level of DNA methyltransferase 1 (DNMT1) in fat tissue might play important role in regulating the changes of methylation pattern on Glut4 and Leptin genes, and which might be one of the molecular mechanisms for the adiposis development.</description><identifier>ISSN: 0862-8408</identifier><identifier>EISSN: 1802-9973</identifier><identifier>DOI: 10.33549/physiolres.933830</identifier><identifier>PMID: 30433796</identifier><language>eng</language><publisher>Czech Republic: Institute of Physiology</publisher><subject>Diabetes mellitus ; Diabetes mellitus (non-insulin dependent) ; DNA methylation ; DNA methyltransferase ; DNMT1 protein ; Epigenetics ; Gene expression ; High fat diet ; Insulin resistance ; Leptin ; Molecular modelling ; Obesity ; Sucrose ; Transcription</subject><ispartof>Physiological research, 2019-01, Vol.68 (1), p.75-87</ispartof><rights>Copyright Institute of Physiology 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c342t-ce5776f5775a6a1cdf03d69d3b901621c360f60ae48f7a53e29d6fb4236f99953</citedby><cites>FETCH-LOGICAL-c342t-ce5776f5775a6a1cdf03d69d3b901621c360f60ae48f7a53e29d6fb4236f99953</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,864,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30433796$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, X</creatorcontrib><creatorcontrib>Tu, P</creatorcontrib><creatorcontrib>Umar, M</creatorcontrib><creatorcontrib>Liu, Q</creatorcontrib><creatorcontrib>Luo, W</creatorcontrib><creatorcontrib>Yang, X</creatorcontrib><creatorcontrib>Zhu, J</creatorcontrib><creatorcontrib>Kong, D</creatorcontrib><creatorcontrib>Li, M</creatorcontrib><title>A study on molecular mechanisms of adiposis induced by long-term treatment of high-fat and high-sucrose in C57BL/6J mice</title><title>Physiological research</title><addtitle>Physiol Res</addtitle><description>Adiposis is reputed as a twin disease of type 2 diabetes and greatly harmful to human health. In order to understand the molecular mechanisms of adiposis, the changes of physiological, pathological, epigenetic and correlative gene expression were investigated during the adiposis development of C57BL/6J mice induced by long time (9 months) high-fat and high-sucrose diet (HFSD) sustainably. The results showed that mRNA transcription level of the Leptin, Glut4 and Glut2 genes have been obviously changed, which exhibit a negative correlation with methylation on their promoter DNA. The results also revealed that HFSD induced higher level of DNA methyltransferase 1 (DNMT1) in fat tissue might play important role in regulating the changes of methylation pattern on Glut4 and Leptin genes, and which might be one of the molecular mechanisms for the adiposis development.</description><subject>Diabetes mellitus</subject><subject>Diabetes mellitus (non-insulin dependent)</subject><subject>DNA methylation</subject><subject>DNA methyltransferase</subject><subject>DNMT1 protein</subject><subject>Epigenetics</subject><subject>Gene expression</subject><subject>High fat diet</subject><subject>Insulin resistance</subject><subject>Leptin</subject><subject>Molecular modelling</subject><subject>Obesity</subject><subject>Sucrose</subject><subject>Transcription</subject><issn>0862-8408</issn><issn>1802-9973</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpFkEtPwzAQhC0EoqXwBzggS5xDHW9ix8dS8VQlLnCOHD-aVElc7EQi_56UFLjsaqWZ2dGH0HVM7gDSRCz35RAqV3sT7gRABuQEzeOM0EgIDqdoTjJGoywh2QxdhLAjhHLC4RzNgCQAXLA5-lrh0PV6wK7FjauN6mvpcWNUKdsqNAE7i6Wu9i5UAVet7pXRuBhw7dpt1Bnf4M4b2TWm7Q7SstqWkZUdlq2ejtAr74IZvXid8vvNkr3iplLmEp1ZWQdzddwL9PH48L5-jjZvTy_r1SZSkNAuUiblnNlxpJLJWGlLQDOhoRAkZjRWwIhlRJoks1ymYKjQzBYJBWaFECks0O2Uu_fuszehy3eu9-34Mqex4DEXkCSjik6qQ9ngjc33vmqkH_KY5D-w83_Y-QR7NN0co_uiMfrP8ksXvgH8pX15</recordid><startdate>20190101</startdate><enddate>20190101</enddate><creator>Li, X</creator><creator>Tu, P</creator><creator>Umar, M</creator><creator>Liu, Q</creator><creator>Luo, W</creator><creator>Yang, X</creator><creator>Zhu, J</creator><creator>Kong, D</creator><creator>Li, M</creator><general>Institute of Physiology</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>4T-</scope><scope>4U-</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>BYOGL</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope></search><sort><creationdate>20190101</creationdate><title>A study on molecular mechanisms of adiposis induced by long-term treatment of high-fat and high-sucrose in C57BL/6J mice</title><author>Li, X ; Tu, P ; Umar, M ; Liu, Q ; Luo, W ; Yang, X ; Zhu, J ; Kong, D ; Li, M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c342t-ce5776f5775a6a1cdf03d69d3b901621c360f60ae48f7a53e29d6fb4236f99953</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Diabetes mellitus</topic><topic>Diabetes mellitus (non-insulin dependent)</topic><topic>DNA methylation</topic><topic>DNA methyltransferase</topic><topic>DNMT1 protein</topic><topic>Epigenetics</topic><topic>Gene expression</topic><topic>High fat diet</topic><topic>Insulin resistance</topic><topic>Leptin</topic><topic>Molecular modelling</topic><topic>Obesity</topic><topic>Sucrose</topic><topic>Transcription</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, X</creatorcontrib><creatorcontrib>Tu, P</creatorcontrib><creatorcontrib>Umar, M</creatorcontrib><creatorcontrib>Liu, Q</creatorcontrib><creatorcontrib>Luo, W</creatorcontrib><creatorcontrib>Yang, X</creatorcontrib><creatorcontrib>Zhu, J</creatorcontrib><creatorcontrib>Kong, D</creatorcontrib><creatorcontrib>Li, M</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Docstoc</collection><collection>University Readers</collection><collection>Proquest Nursing & Allied Health Source</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>East Europe, Central Europe Database</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</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><jtitle>Physiological research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, X</au><au>Tu, P</au><au>Umar, M</au><au>Liu, Q</au><au>Luo, W</au><au>Yang, X</au><au>Zhu, J</au><au>Kong, D</au><au>Li, M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A study on molecular mechanisms of adiposis induced by long-term treatment of high-fat and high-sucrose in C57BL/6J mice</atitle><jtitle>Physiological research</jtitle><addtitle>Physiol Res</addtitle><date>2019-01-01</date><risdate>2019</risdate><volume>68</volume><issue>1</issue><spage>75</spage><epage>87</epage><pages>75-87</pages><issn>0862-8408</issn><eissn>1802-9973</eissn><abstract>Adiposis is reputed as a twin disease of type 2 diabetes and greatly harmful to human health. 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| subjects | Diabetes mellitus Diabetes mellitus (non-insulin dependent) DNA methylation DNA methyltransferase DNMT1 protein Epigenetics Gene expression High fat diet Insulin resistance Leptin Molecular modelling Obesity Sucrose Transcription |
| title | A study on molecular mechanisms of adiposis induced by long-term treatment of high-fat and high-sucrose in C57BL/6J mice |
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