Glucose fluctuations increase the incidence of atrial fibrillation in diabetic rats
We investigated whether glucose fluctuations aggravate cardiac fibrosis and increase the occurrence of atrial fibrillation (AF) in rats with diabetes mellitus (DM). Streptozotocin-induced diabetic rats were randomly divided into three groups: uncontrolled DM (U-STZ) group, controlled DM (C-STZ) grou...
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| Veröffentlicht in: | Cardiovascular research 2014-10, Vol.104 (1), p.5-14 |
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| creator | Saito, Shotaro Teshima, Yasushi Fukui, Akira Kondo, Hidekazu Nishio, Satoru Nakagawa, Mikiko Saikawa, Tetsunori Takahashi, Naohiko |
| description | We investigated whether glucose fluctuations aggravate cardiac fibrosis and increase the occurrence of atrial fibrillation (AF) in rats with diabetes mellitus (DM).
Streptozotocin-induced diabetic rats were randomly divided into three groups: uncontrolled DM (U-STZ) group, controlled DM (C-STZ) group, and DM with glucose fluctuations (STZ-GF) group. Glucose fluctuations were induced by fasting for 24 h and additional regular insulin injections (0.5 IU/kg) administered three times per week for three consecutive weeks. C-STZ rats were administered long acting insulin (20 IU/kg) twice a day to control blood glucose levels. Cardiac fibrosis evaluated by Masson trichrome staining and the expressions of collagen type 1, collagen type 3, and α-smooth muscle actin were increased in U-STZ rats compared with C-STZ rats, which were more pronounced in STZ-GF rats. The inducibility of AF was significantly larger in U-STZ rats than C-STZ rats and was greatest in STZ-GF rats. To explore the mechanism of cardiac fibrosis, we investigated the levels of reactive oxygen species (ROS) and apoptosis. The expression of malondialdehyde, an indicator of ROS levels, was significantly upregulated in STZ-GF rats compared with U-STZ rats, along with increased thioredoxin-interacting protein (Txnip) expression in STZ-GF rats. Furthermore, caspase-3 expression and the number of TUNEL-positive cells were significantly increased in STZ-GF rats compared with U-STZ and C-STZ rats.
Glucose fluctuations increase the incidence of AF by promoting cardiac fibrosis. Increased ROS levels caused by upregulation of Txnip expression may be a mechanism whereby in glucose fluctuations induce fibrosis. |
| doi_str_mv | 10.1093/cvr/cvu176 |
| format | Article |
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Streptozotocin-induced diabetic rats were randomly divided into three groups: uncontrolled DM (U-STZ) group, controlled DM (C-STZ) group, and DM with glucose fluctuations (STZ-GF) group. Glucose fluctuations were induced by fasting for 24 h and additional regular insulin injections (0.5 IU/kg) administered three times per week for three consecutive weeks. C-STZ rats were administered long acting insulin (20 IU/kg) twice a day to control blood glucose levels. Cardiac fibrosis evaluated by Masson trichrome staining and the expressions of collagen type 1, collagen type 3, and α-smooth muscle actin were increased in U-STZ rats compared with C-STZ rats, which were more pronounced in STZ-GF rats. The inducibility of AF was significantly larger in U-STZ rats than C-STZ rats and was greatest in STZ-GF rats. To explore the mechanism of cardiac fibrosis, we investigated the levels of reactive oxygen species (ROS) and apoptosis. The expression of malondialdehyde, an indicator of ROS levels, was significantly upregulated in STZ-GF rats compared with U-STZ rats, along with increased thioredoxin-interacting protein (Txnip) expression in STZ-GF rats. Furthermore, caspase-3 expression and the number of TUNEL-positive cells were significantly increased in STZ-GF rats compared with U-STZ and C-STZ rats.
Glucose fluctuations increase the incidence of AF by promoting cardiac fibrosis. Increased ROS levels caused by upregulation of Txnip expression may be a mechanism whereby in glucose fluctuations induce fibrosis.</description><identifier>ISSN: 0008-6363</identifier><identifier>EISSN: 1755-3245</identifier><identifier>DOI: 10.1093/cvr/cvu176</identifier><identifier>PMID: 25082849</identifier><language>eng</language><publisher>England</publisher><subject>Actins - metabolism ; Action Potentials ; Animals ; Apoptosis ; Atrial Fibrillation - blood ; Atrial Fibrillation - etiology ; Atrial Fibrillation - pathology ; Atrial Fibrillation - physiopathology ; Biomarkers - blood ; Blood Glucose - drug effects ; Blood Glucose - metabolism ; Carrier Proteins - metabolism ; Caspase 3 - metabolism ; Cells, Cultured ; Collagen Type I - metabolism ; Collagen Type III - metabolism ; Diabetes Mellitus, Experimental - blood ; Diabetes Mellitus, Experimental - complications ; Diabetes Mellitus, Experimental - drug therapy ; Diabetic Cardiomyopathies - blood ; Diabetic Cardiomyopathies - etiology ; Diabetic Cardiomyopathies - pathology ; Diabetic Cardiomyopathies - physiopathology ; Fibrosis ; Hypoglycemic Agents - pharmacology ; Insulin, Long-Acting - pharmacology ; Male ; Malondialdehyde - metabolism ; Myocardium - metabolism ; Myocardium - pathology ; Oxidative Stress ; Rats, Sprague-Dawley ; Reactive Oxygen Species - metabolism ; Refractory Period, Electrophysiological ; Signal Transduction ; Time Factors ; Ventricular Dysfunction, Left - etiology ; Ventricular Dysfunction, Left - metabolism ; Ventricular Dysfunction, Left - physiopathology ; Ventricular Function, Left</subject><ispartof>Cardiovascular research, 2014-10, Vol.104 (1), p.5-14</ispartof><rights>Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2014. For permissions please email: journals.permissions@oup.com.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c408t-f814daf7aeed101dbbf5e2a20cc23b2f6c7301b8b6847a4782e13a0d74ea015e3</citedby><cites>FETCH-LOGICAL-c408t-f814daf7aeed101dbbf5e2a20cc23b2f6c7301b8b6847a4782e13a0d74ea015e3</cites></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/25082849$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Saito, Shotaro</creatorcontrib><creatorcontrib>Teshima, Yasushi</creatorcontrib><creatorcontrib>Fukui, Akira</creatorcontrib><creatorcontrib>Kondo, Hidekazu</creatorcontrib><creatorcontrib>Nishio, Satoru</creatorcontrib><creatorcontrib>Nakagawa, Mikiko</creatorcontrib><creatorcontrib>Saikawa, Tetsunori</creatorcontrib><creatorcontrib>Takahashi, Naohiko</creatorcontrib><title>Glucose fluctuations increase the incidence of atrial fibrillation in diabetic rats</title><title>Cardiovascular research</title><addtitle>Cardiovasc Res</addtitle><description>We investigated whether glucose fluctuations aggravate cardiac fibrosis and increase the occurrence of atrial fibrillation (AF) in rats with diabetes mellitus (DM).
Streptozotocin-induced diabetic rats were randomly divided into three groups: uncontrolled DM (U-STZ) group, controlled DM (C-STZ) group, and DM with glucose fluctuations (STZ-GF) group. Glucose fluctuations were induced by fasting for 24 h and additional regular insulin injections (0.5 IU/kg) administered three times per week for three consecutive weeks. C-STZ rats were administered long acting insulin (20 IU/kg) twice a day to control blood glucose levels. Cardiac fibrosis evaluated by Masson trichrome staining and the expressions of collagen type 1, collagen type 3, and α-smooth muscle actin were increased in U-STZ rats compared with C-STZ rats, which were more pronounced in STZ-GF rats. The inducibility of AF was significantly larger in U-STZ rats than C-STZ rats and was greatest in STZ-GF rats. To explore the mechanism of cardiac fibrosis, we investigated the levels of reactive oxygen species (ROS) and apoptosis. The expression of malondialdehyde, an indicator of ROS levels, was significantly upregulated in STZ-GF rats compared with U-STZ rats, along with increased thioredoxin-interacting protein (Txnip) expression in STZ-GF rats. Furthermore, caspase-3 expression and the number of TUNEL-positive cells were significantly increased in STZ-GF rats compared with U-STZ and C-STZ rats.
Glucose fluctuations increase the incidence of AF by promoting cardiac fibrosis. Increased ROS levels caused by upregulation of Txnip expression may be a mechanism whereby in glucose fluctuations induce fibrosis.</description><subject>Actins - metabolism</subject><subject>Action Potentials</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Atrial Fibrillation - blood</subject><subject>Atrial Fibrillation - etiology</subject><subject>Atrial Fibrillation - pathology</subject><subject>Atrial Fibrillation - physiopathology</subject><subject>Biomarkers - blood</subject><subject>Blood Glucose - drug effects</subject><subject>Blood Glucose - metabolism</subject><subject>Carrier Proteins - metabolism</subject><subject>Caspase 3 - metabolism</subject><subject>Cells, Cultured</subject><subject>Collagen Type I - metabolism</subject><subject>Collagen Type III - metabolism</subject><subject>Diabetes Mellitus, Experimental - blood</subject><subject>Diabetes Mellitus, Experimental - complications</subject><subject>Diabetes Mellitus, Experimental - drug therapy</subject><subject>Diabetic Cardiomyopathies - blood</subject><subject>Diabetic Cardiomyopathies - etiology</subject><subject>Diabetic Cardiomyopathies - pathology</subject><subject>Diabetic Cardiomyopathies - physiopathology</subject><subject>Fibrosis</subject><subject>Hypoglycemic Agents - pharmacology</subject><subject>Insulin, Long-Acting - pharmacology</subject><subject>Male</subject><subject>Malondialdehyde - metabolism</subject><subject>Myocardium - metabolism</subject><subject>Myocardium - pathology</subject><subject>Oxidative Stress</subject><subject>Rats, Sprague-Dawley</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Refractory Period, Electrophysiological</subject><subject>Signal Transduction</subject><subject>Time Factors</subject><subject>Ventricular Dysfunction, Left - etiology</subject><subject>Ventricular Dysfunction, Left - metabolism</subject><subject>Ventricular Dysfunction, Left - physiopathology</subject><subject>Ventricular Function, Left</subject><issn>0008-6363</issn><issn>1755-3245</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kE1LAzEQhoMotlYv_gDZowirmXxs0qMUrULBg3pekuwEI9tuTbKC_95oq4fhZYaHl-Eh5BzoNdA5v3GfscwIqjkgU1BS1pwJeUimlFJdN7zhE3KS0ntZpVTimEyYpJppMZ-S52U_uiFh5Uvm0eQwbFIVNi6iKdf8hj9L6HDjsBp8ZXIMpq98sDH0_S9egKoLxmIOroomp1Ny5E2f8GyfM_J6f_eyeKhXT8vHxe2qdoLqXHsNojNeGcQOKHTWeonMMOoc45b5xilOwWrbaKGMUJohcEM7JdBQkMhn5HLXu43Dx4gpt-uQHJa3NjiMqQXZNAAgQRX0aoe6OKQU0bfbGNYmfrVA2x-JbZHY7iQW-GLfO9o1dv_onzX-DXGvb4E</recordid><startdate>20141001</startdate><enddate>20141001</enddate><creator>Saito, Shotaro</creator><creator>Teshima, Yasushi</creator><creator>Fukui, Akira</creator><creator>Kondo, Hidekazu</creator><creator>Nishio, Satoru</creator><creator>Nakagawa, Mikiko</creator><creator>Saikawa, Tetsunori</creator><creator>Takahashi, Naohiko</creator><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>20141001</creationdate><title>Glucose fluctuations increase the incidence of atrial fibrillation in diabetic rats</title><author>Saito, Shotaro ; Teshima, Yasushi ; Fukui, Akira ; Kondo, Hidekazu ; Nishio, Satoru ; Nakagawa, Mikiko ; Saikawa, Tetsunori ; Takahashi, Naohiko</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c408t-f814daf7aeed101dbbf5e2a20cc23b2f6c7301b8b6847a4782e13a0d74ea015e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Actins - metabolism</topic><topic>Action Potentials</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Atrial Fibrillation - blood</topic><topic>Atrial Fibrillation - etiology</topic><topic>Atrial Fibrillation - pathology</topic><topic>Atrial Fibrillation - physiopathology</topic><topic>Biomarkers - blood</topic><topic>Blood Glucose - drug effects</topic><topic>Blood Glucose - metabolism</topic><topic>Carrier Proteins - metabolism</topic><topic>Caspase 3 - metabolism</topic><topic>Cells, Cultured</topic><topic>Collagen Type I - metabolism</topic><topic>Collagen Type III - metabolism</topic><topic>Diabetes Mellitus, Experimental - blood</topic><topic>Diabetes Mellitus, Experimental - complications</topic><topic>Diabetes Mellitus, Experimental - drug therapy</topic><topic>Diabetic Cardiomyopathies - blood</topic><topic>Diabetic Cardiomyopathies - etiology</topic><topic>Diabetic Cardiomyopathies - pathology</topic><topic>Diabetic Cardiomyopathies - physiopathology</topic><topic>Fibrosis</topic><topic>Hypoglycemic Agents - pharmacology</topic><topic>Insulin, Long-Acting - pharmacology</topic><topic>Male</topic><topic>Malondialdehyde - metabolism</topic><topic>Myocardium - metabolism</topic><topic>Myocardium - pathology</topic><topic>Oxidative Stress</topic><topic>Rats, Sprague-Dawley</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Refractory Period, Electrophysiological</topic><topic>Signal Transduction</topic><topic>Time Factors</topic><topic>Ventricular Dysfunction, Left - etiology</topic><topic>Ventricular Dysfunction, Left - metabolism</topic><topic>Ventricular Dysfunction, Left - physiopathology</topic><topic>Ventricular Function, Left</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Saito, Shotaro</creatorcontrib><creatorcontrib>Teshima, Yasushi</creatorcontrib><creatorcontrib>Fukui, Akira</creatorcontrib><creatorcontrib>Kondo, Hidekazu</creatorcontrib><creatorcontrib>Nishio, Satoru</creatorcontrib><creatorcontrib>Nakagawa, Mikiko</creatorcontrib><creatorcontrib>Saikawa, Tetsunori</creatorcontrib><creatorcontrib>Takahashi, Naohiko</creatorcontrib><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>Cardiovascular research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Saito, Shotaro</au><au>Teshima, Yasushi</au><au>Fukui, Akira</au><au>Kondo, Hidekazu</au><au>Nishio, Satoru</au><au>Nakagawa, Mikiko</au><au>Saikawa, Tetsunori</au><au>Takahashi, Naohiko</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Glucose fluctuations increase the incidence of atrial fibrillation in diabetic rats</atitle><jtitle>Cardiovascular research</jtitle><addtitle>Cardiovasc Res</addtitle><date>2014-10-01</date><risdate>2014</risdate><volume>104</volume><issue>1</issue><spage>5</spage><epage>14</epage><pages>5-14</pages><issn>0008-6363</issn><eissn>1755-3245</eissn><abstract>We investigated whether glucose fluctuations aggravate cardiac fibrosis and increase the occurrence of atrial fibrillation (AF) in rats with diabetes mellitus (DM).
Streptozotocin-induced diabetic rats were randomly divided into three groups: uncontrolled DM (U-STZ) group, controlled DM (C-STZ) group, and DM with glucose fluctuations (STZ-GF) group. Glucose fluctuations were induced by fasting for 24 h and additional regular insulin injections (0.5 IU/kg) administered three times per week for three consecutive weeks. C-STZ rats were administered long acting insulin (20 IU/kg) twice a day to control blood glucose levels. Cardiac fibrosis evaluated by Masson trichrome staining and the expressions of collagen type 1, collagen type 3, and α-smooth muscle actin were increased in U-STZ rats compared with C-STZ rats, which were more pronounced in STZ-GF rats. The inducibility of AF was significantly larger in U-STZ rats than C-STZ rats and was greatest in STZ-GF rats. To explore the mechanism of cardiac fibrosis, we investigated the levels of reactive oxygen species (ROS) and apoptosis. The expression of malondialdehyde, an indicator of ROS levels, was significantly upregulated in STZ-GF rats compared with U-STZ rats, along with increased thioredoxin-interacting protein (Txnip) expression in STZ-GF rats. Furthermore, caspase-3 expression and the number of TUNEL-positive cells were significantly increased in STZ-GF rats compared with U-STZ and C-STZ rats.
Glucose fluctuations increase the incidence of AF by promoting cardiac fibrosis. Increased ROS levels caused by upregulation of Txnip expression may be a mechanism whereby in glucose fluctuations induce fibrosis.</abstract><cop>England</cop><pmid>25082849</pmid><doi>10.1093/cvr/cvu176</doi><tpages>10</tpages></addata></record> |
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| subjects | Actins - metabolism Action Potentials Animals Apoptosis Atrial Fibrillation - blood Atrial Fibrillation - etiology Atrial Fibrillation - pathology Atrial Fibrillation - physiopathology Biomarkers - blood Blood Glucose - drug effects Blood Glucose - metabolism Carrier Proteins - metabolism Caspase 3 - metabolism Cells, Cultured Collagen Type I - metabolism Collagen Type III - metabolism Diabetes Mellitus, Experimental - blood Diabetes Mellitus, Experimental - complications Diabetes Mellitus, Experimental - drug therapy Diabetic Cardiomyopathies - blood Diabetic Cardiomyopathies - etiology Diabetic Cardiomyopathies - pathology Diabetic Cardiomyopathies - physiopathology Fibrosis Hypoglycemic Agents - pharmacology Insulin, Long-Acting - pharmacology Male Malondialdehyde - metabolism Myocardium - metabolism Myocardium - pathology Oxidative Stress Rats, Sprague-Dawley Reactive Oxygen Species - metabolism Refractory Period, Electrophysiological Signal Transduction Time Factors Ventricular Dysfunction, Left - etiology Ventricular Dysfunction, Left - metabolism Ventricular Dysfunction, Left - physiopathology Ventricular Function, Left |
| title | Glucose fluctuations increase the incidence of atrial fibrillation in diabetic rats |
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