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...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Clinical and experimental hypertension (1993) 2009-01, Vol.31 (3), p.201-207
Hauptverfasser: Ando, Hitoshi, Ushijima, Kentarou, Yanagihara, Hayato, Hayashi, Yohei, Takamura, Toshinari, Kaneko, Shuichi, Fujimura, Akio
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 207
container_issue 3
container_start_page 201
container_title Clinical and experimental hypertension (1993)
container_volume 31
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
format Article
fullrecord <record><control><sourceid>proquest_infor</sourceid><recordid>TN_cdi_informahealthcare_journals_10_1080_10641960902822450</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>67150184</sourcerecordid><originalsourceid>FETCH-LOGICAL-c500t-2a69bddca955addb3caef39ded4235cea2dee876e7475b4ff27f77571257b5333</originalsourceid><addsrcrecordid>eNp9kE1vFDEMhiMEoqXwA7igXOA2kI9JMiO4VEtZKlathMp55EkcbdrZyZDMAsuvJ9UuRahSD5Yt-3kt-yXkJWdvOWvYO850zVvNWiYaIWrFHpFjroSqNGP6canLvCqAPCLPcr5mjNdaNU_JEW9lY5pWHxO_GKK9oUsckZ79mhLmHOJIw0jnNdJV-IGJwujoqQtTzEivQs5bzDR6ehHH6rLH2-ZuQiroxwA9zsHSZZxj9QVuwu8S9CvM-Tl54mHI-OKQT8i3T2dXi8_V6nJ5vjhdVVYxNlcCdNs7Z6FVCpzrpQX0snXoaiGVRRAOsTEaTW1UX3svjDdGGS6U6ZWU8oS82e-dUvxe7py7TcgWhwFGjNvcacMV401dQL4HbYo5J_TdlMIG0q7jrLs1t7tnbtG8Oizf9ht0_xQHNwvw-gBAtjD4BKMN-Y4TXLdSa164D3sujD6mDfyMaXDdDLshpr8i-dAd7_-TrxGGeW0hYXcdt2ksBj_wxR_OQKZR</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>67150184</pqid></control><display><type>article</type><title>Clock Gene Expression in the Liver and Adipose Tissues of Non-Obese Type 2 Diabetic Goto-Kakizaki Rats</title><source>MEDLINE</source><source>Taylor &amp; Francis Journals Complete</source><creator>Ando, Hitoshi ; Ushijima, Kentarou ; Yanagihara, Hayato ; Hayashi, Yohei ; Takamura, Toshinari ; Kaneko, Shuichi ; Fujimura, Akio</creator><creatorcontrib>Ando, Hitoshi ; Ushijima, Kentarou ; Yanagihara, Hayato ; Hayashi, Yohei ; Takamura, Toshinari ; Kaneko, Shuichi ; Fujimura, Akio</creatorcontrib><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><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&amp;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 &amp; 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>
fulltext fulltext
identifier ISSN: 1064-1963
ispartof Clinical and experimental hypertension (1993), 2009-01, Vol.31 (3), p.201-207
issn 1064-1963
1525-6006
language eng
recordid cdi_informahealthcare_journals_10_1080_10641960902822450
source MEDLINE; Taylor & Francis Journals Complete
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
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-26T13%3A33%3A09IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_infor&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Clock%20Gene%20Expression%20in%20the%20Liver%20and%20Adipose%20Tissues%20of%20Non-Obese%20Type%202%20Diabetic%20Goto-Kakizaki%20Rats&rft.jtitle=Clinical%20and%20experimental%20hypertension%20(1993)&rft.au=Ando,%20Hitoshi&rft.date=2009-01-01&rft.volume=31&rft.issue=3&rft.spage=201&rft.epage=207&rft.pages=201-207&rft.issn=1064-1963&rft.eissn=1525-6006&rft.coden=CEHYER&rft_id=info:doi/10.1080/10641960902822450&rft_dat=%3Cproquest_infor%3E67150184%3C/proquest_infor%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=67150184&rft_id=info:pmid/19387896&rfr_iscdi=true