Clock Gene Expression in the Liver and Adipose Tissues of Non-Obese Type 2 Diabetic Goto-Kakizaki Rats
Recent studies have revealed a close relationship between the pathophysiology of metabolic syndrome, which is characterized by obesity and hyperglycemia, and the functioning of internal molecular clocks. In this study, we show that the rhythmic mRNA expression of clock genes (Clock, Bmal1, Cry1, and...
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Veröffentlicht in: | Clinical and experimental hypertension (1993) 2009-01, Vol.31 (3), p.201-207 |
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container_title | Clinical and experimental hypertension (1993) |
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creator | Ando, Hitoshi Ushijima, Kentarou Yanagihara, Hayato Hayashi, Yohei Takamura, Toshinari Kaneko, Shuichi Fujimura, Akio |
description | Recent studies have revealed a close relationship between the pathophysiology of metabolic syndrome, which is characterized by obesity and hyperglycemia, and the functioning of internal molecular clocks. In this study, we show that the rhythmic mRNA expression of clock genes (Clock, Bmal1, Cry1, and Dbp) is not attenuated in the liver and visceral adipose tissues of Goto-Kakizaki rats, a model of nonobese, type 2 diabetes, as compared to control Wistar rats. Our results suggest that molecular clock impairment in peripheral tissues of obese diabetic animals may be either caused by obesity-related factor(s), but not hyperglycemia, or be a cause, but not a consequence, of hyperglycemia. |
doi_str_mv | 10.1080/10641960902822450 |
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In this study, we show that the rhythmic mRNA expression of clock genes (Clock, Bmal1, Cry1, and Dbp) is not attenuated in the liver and visceral adipose tissues of Goto-Kakizaki rats, a model of nonobese, type 2 diabetes, as compared to control Wistar rats. Our results suggest that molecular clock impairment in peripheral tissues of obese diabetic animals may be either caused by obesity-related factor(s), but not hyperglycemia, or be a cause, but not a consequence, of hyperglycemia.</description><identifier>ISSN: 1064-1963</identifier><identifier>EISSN: 1525-6006</identifier><identifier>DOI: 10.1080/10641960902822450</identifier><identifier>PMID: 19387896</identifier><identifier>CODEN: CEHYER</identifier><language>eng</language><publisher>Colchester: Informa UK Ltd</publisher><subject>Adipose Tissue - metabolism ; Animals ; ARNTL Transcription Factors ; Arterial hypertension. Arterial hypotension ; Basic Helix-Loop-Helix Transcription Factors - metabolism ; Biological and medical sciences ; Blood and lymphatic vessels ; Blood Glucose - metabolism ; Cardiology. Vascular system ; Circadian Rhythm ; clock gene ; CLOCK Proteins ; Cryptochromes ; Diabetes Mellitus, Type 2 - metabolism ; Disease Models, Animal ; DNA-Binding Proteins ; Experimental diseases ; Flavoproteins - metabolism ; Insulin - blood ; liver ; Liver - metabolism ; Male ; Medical sciences ; metabolic syndrome ; Rats ; Rats, Mutant Strains ; Rats, Wistar ; RNA, Messenger - metabolism ; Trans-Activators - metabolism ; Transcription Factors ; type 2 diabetes</subject><ispartof>Clinical and experimental hypertension (1993), 2009-01, Vol.31 (3), p.201-207</ispartof><rights>2009 Informa UK Ltd All rights reserved: reproduction in whole or part not permitted 2009</rights><rights>2009 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c500t-2a69bddca955addb3caef39ded4235cea2dee876e7475b4ff27f77571257b5333</citedby><cites>FETCH-LOGICAL-c500t-2a69bddca955addb3caef39ded4235cea2dee876e7475b4ff27f77571257b5333</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.tandfonline.com/doi/pdf/10.1080/10641960902822450$$EPDF$$P50$$Ginformaworld$$H</linktopdf><linktohtml>$$Uhttps://www.tandfonline.com/doi/full/10.1080/10641960902822450$$EHTML$$P50$$Ginformaworld$$H</linktohtml><link.rule.ids>309,310,314,776,780,785,786,23910,23911,25119,27903,27904,59623,60412,61197,61378</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21693661$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19387896$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ando, Hitoshi</creatorcontrib><creatorcontrib>Ushijima, Kentarou</creatorcontrib><creatorcontrib>Yanagihara, Hayato</creatorcontrib><creatorcontrib>Hayashi, Yohei</creatorcontrib><creatorcontrib>Takamura, Toshinari</creatorcontrib><creatorcontrib>Kaneko, Shuichi</creatorcontrib><creatorcontrib>Fujimura, Akio</creatorcontrib><title>Clock Gene Expression in the Liver and Adipose Tissues of Non-Obese Type 2 Diabetic Goto-Kakizaki Rats</title><title>Clinical and experimental hypertension (1993)</title><addtitle>Clin Exp Hypertens</addtitle><description>Recent studies have revealed a close relationship between the pathophysiology of metabolic syndrome, which is characterized by obesity and hyperglycemia, and the functioning of internal molecular clocks. In this study, we show that the rhythmic mRNA expression of clock genes (Clock, Bmal1, Cry1, and Dbp) is not attenuated in the liver and visceral adipose tissues of Goto-Kakizaki rats, a model of nonobese, type 2 diabetes, as compared to control Wistar rats. Our results suggest that molecular clock impairment in peripheral tissues of obese diabetic animals may be either caused by obesity-related factor(s), but not hyperglycemia, or be a cause, but not a consequence, of hyperglycemia.</description><subject>Adipose Tissue - metabolism</subject><subject>Animals</subject><subject>ARNTL Transcription Factors</subject><subject>Arterial hypertension. Arterial hypotension</subject><subject>Basic Helix-Loop-Helix Transcription Factors - metabolism</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Blood Glucose - metabolism</subject><subject>Cardiology. Vascular system</subject><subject>Circadian Rhythm</subject><subject>clock gene</subject><subject>CLOCK Proteins</subject><subject>Cryptochromes</subject><subject>Diabetes Mellitus, Type 2 - metabolism</subject><subject>Disease Models, Animal</subject><subject>DNA-Binding Proteins</subject><subject>Experimental diseases</subject><subject>Flavoproteins - metabolism</subject><subject>Insulin - blood</subject><subject>liver</subject><subject>Liver - metabolism</subject><subject>Male</subject><subject>Medical sciences</subject><subject>metabolic syndrome</subject><subject>Rats</subject><subject>Rats, Mutant Strains</subject><subject>Rats, Wistar</subject><subject>RNA, Messenger - metabolism</subject><subject>Trans-Activators - metabolism</subject><subject>Transcription Factors</subject><subject>type 2 diabetes</subject><issn>1064-1963</issn><issn>1525-6006</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1vFDEMhiMEoqXwA7igXOA2kI9JMiO4VEtZKlathMp55EkcbdrZyZDMAsuvJ9UuRahSD5Yt-3kt-yXkJWdvOWvYO850zVvNWiYaIWrFHpFjroSqNGP6canLvCqAPCLPcr5mjNdaNU_JEW9lY5pWHxO_GKK9oUsckZ79mhLmHOJIw0jnNdJV-IGJwujoqQtTzEivQs5bzDR6ehHH6rLH2-ZuQiroxwA9zsHSZZxj9QVuwu8S9CvM-Tl54mHI-OKQT8i3T2dXi8_V6nJ5vjhdVVYxNlcCdNs7Z6FVCpzrpQX0snXoaiGVRRAOsTEaTW1UX3svjDdGGS6U6ZWU8oS82e-dUvxe7py7TcgWhwFGjNvcacMV401dQL4HbYo5J_TdlMIG0q7jrLs1t7tnbtG8Oizf9ht0_xQHNwvw-gBAtjD4BKMN-Y4TXLdSa164D3sujD6mDfyMaXDdDLshpr8i-dAd7_-TrxGGeW0hYXcdt2ksBj_wxR_OQKZR</recordid><startdate>20090101</startdate><enddate>20090101</enddate><creator>Ando, Hitoshi</creator><creator>Ushijima, Kentarou</creator><creator>Yanagihara, Hayato</creator><creator>Hayashi, Yohei</creator><creator>Takamura, Toshinari</creator><creator>Kaneko, Shuichi</creator><creator>Fujimura, Akio</creator><general>Informa UK Ltd</general><general>Taylor & Francis</general><scope>IQODW</scope><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>7X8</scope></search><sort><creationdate>20090101</creationdate><title>Clock Gene Expression in the Liver and Adipose Tissues of Non-Obese Type 2 Diabetic Goto-Kakizaki Rats</title><author>Ando, Hitoshi ; Ushijima, Kentarou ; Yanagihara, Hayato ; Hayashi, Yohei ; Takamura, Toshinari ; Kaneko, Shuichi ; Fujimura, Akio</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c500t-2a69bddca955addb3caef39ded4235cea2dee876e7475b4ff27f77571257b5333</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Adipose Tissue - metabolism</topic><topic>Animals</topic><topic>ARNTL Transcription Factors</topic><topic>Arterial hypertension. Arterial hypotension</topic><topic>Basic Helix-Loop-Helix Transcription Factors - metabolism</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Blood Glucose - metabolism</topic><topic>Cardiology. Vascular system</topic><topic>Circadian Rhythm</topic><topic>clock gene</topic><topic>CLOCK Proteins</topic><topic>Cryptochromes</topic><topic>Diabetes Mellitus, Type 2 - metabolism</topic><topic>Disease Models, Animal</topic><topic>DNA-Binding Proteins</topic><topic>Experimental diseases</topic><topic>Flavoproteins - metabolism</topic><topic>Insulin - blood</topic><topic>liver</topic><topic>Liver - metabolism</topic><topic>Male</topic><topic>Medical sciences</topic><topic>metabolic syndrome</topic><topic>Rats</topic><topic>Rats, Mutant Strains</topic><topic>Rats, Wistar</topic><topic>RNA, Messenger - metabolism</topic><topic>Trans-Activators - metabolism</topic><topic>Transcription Factors</topic><topic>type 2 diabetes</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ando, Hitoshi</creatorcontrib><creatorcontrib>Ushijima, Kentarou</creatorcontrib><creatorcontrib>Yanagihara, Hayato</creatorcontrib><creatorcontrib>Hayashi, Yohei</creatorcontrib><creatorcontrib>Takamura, Toshinari</creatorcontrib><creatorcontrib>Kaneko, Shuichi</creatorcontrib><creatorcontrib>Fujimura, Akio</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Clinical and experimental hypertension (1993)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ando, Hitoshi</au><au>Ushijima, Kentarou</au><au>Yanagihara, Hayato</au><au>Hayashi, Yohei</au><au>Takamura, Toshinari</au><au>Kaneko, Shuichi</au><au>Fujimura, Akio</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Clock Gene Expression in the Liver and Adipose Tissues of Non-Obese Type 2 Diabetic Goto-Kakizaki Rats</atitle><jtitle>Clinical and experimental hypertension (1993)</jtitle><addtitle>Clin Exp Hypertens</addtitle><date>2009-01-01</date><risdate>2009</risdate><volume>31</volume><issue>3</issue><spage>201</spage><epage>207</epage><pages>201-207</pages><issn>1064-1963</issn><eissn>1525-6006</eissn><coden>CEHYER</coden><abstract>Recent studies have revealed a close relationship between the pathophysiology of metabolic syndrome, which is characterized by obesity and hyperglycemia, and the functioning of internal molecular clocks. In this study, we show that the rhythmic mRNA expression of clock genes (Clock, Bmal1, Cry1, and Dbp) is not attenuated in the liver and visceral adipose tissues of Goto-Kakizaki rats, a model of nonobese, type 2 diabetes, as compared to control Wistar rats. Our results suggest that molecular clock impairment in peripheral tissues of obese diabetic animals may be either caused by obesity-related factor(s), but not hyperglycemia, or be a cause, but not a consequence, of hyperglycemia.</abstract><cop>Colchester</cop><pub>Informa UK Ltd</pub><pmid>19387896</pmid><doi>10.1080/10641960902822450</doi><tpages>7</tpages></addata></record> |
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subjects | Adipose Tissue - metabolism Animals ARNTL Transcription Factors Arterial hypertension. Arterial hypotension Basic Helix-Loop-Helix Transcription Factors - metabolism Biological and medical sciences Blood and lymphatic vessels Blood Glucose - metabolism Cardiology. Vascular system Circadian Rhythm clock gene CLOCK Proteins Cryptochromes Diabetes Mellitus, Type 2 - metabolism Disease Models, Animal DNA-Binding Proteins Experimental diseases Flavoproteins - metabolism Insulin - blood liver Liver - metabolism Male Medical sciences metabolic syndrome Rats Rats, Mutant Strains Rats, Wistar RNA, Messenger - metabolism Trans-Activators - metabolism Transcription Factors type 2 diabetes |
title | Clock Gene Expression in the Liver and Adipose Tissues of Non-Obese Type 2 Diabetic Goto-Kakizaki Rats |
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