Myocardial infarction in rats causes partial impairment in insulin response associated with reduced fatty acid oxidation and mitochondrial gene expression
Objective Myocardial infarction leads to contractile dysfunction. In patients with diabetes, impaired contractility has been associated with the loss of insulin effects and mitochondrial dysfunction. We assessed cardiac insulin sensitivity and mitochondrial and contractile function in rats after lig...
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| Veröffentlicht in: | The Journal of thoracic and cardiovascular surgery 2010-11, Vol.140 (5), p.1160-1167 |
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| creator | Amorim, Paulo A., MD Nguyen, T. Dung, BS Shingu, Yasushige, MD Schwarzer, Michael, PhD Mohr, Friedrich W., MD, PhD Schrepper, Andrea, MS Doenst, Torsten, MD, PhD |
| description | Objective Myocardial infarction leads to contractile dysfunction. In patients with diabetes, impaired contractility has been associated with the loss of insulin effects and mitochondrial dysfunction. We assessed cardiac insulin sensitivity and mitochondrial and contractile function in rats after ligation of the left coronary artery. Methods At 2 weeks after left coronary artery ligation, we performed echocardiography in vivo and assessed the substrate use and insulin response in the isolated working heart and the regulation of insulin (Akt, glucose transporter type 4) and mitochondrial signaling (p38 mitogen-activated protein kinase, peroxisome proliferator-activated receptor-γ coactivator 1α, mitochondrial transcription factor A) using polymerase chain reaction and Western blotting. Results The infarcted hearts were dilated and had a reduced ejection fraction (ejection fraction |
| doi_str_mv | 10.1016/j.jtcvs.2010.08.003 |
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Dung, BS ; Shingu, Yasushige, MD ; Schwarzer, Michael, PhD ; Mohr, Friedrich W., MD, PhD ; Schrepper, Andrea, MS ; Doenst, Torsten, MD, PhD</creator><creatorcontrib>Amorim, Paulo A., MD ; Nguyen, T. Dung, BS ; Shingu, Yasushige, MD ; Schwarzer, Michael, PhD ; Mohr, Friedrich W., MD, PhD ; Schrepper, Andrea, MS ; Doenst, Torsten, MD, PhD</creatorcontrib><description>Objective Myocardial infarction leads to contractile dysfunction. In patients with diabetes, impaired contractility has been associated with the loss of insulin effects and mitochondrial dysfunction. We assessed cardiac insulin sensitivity and mitochondrial and contractile function in rats after ligation of the left coronary artery. Methods At 2 weeks after left coronary artery ligation, we performed echocardiography in vivo and assessed the substrate use and insulin response in the isolated working heart and the regulation of insulin (Akt, glucose transporter type 4) and mitochondrial signaling (p38 mitogen-activated protein kinase, peroxisome proliferator-activated receptor-γ coactivator 1α, mitochondrial transcription factor A) using polymerase chain reaction and Western blotting. Results The infarcted hearts were dilated and had a reduced ejection fraction (ejection fraction < 50%). The basal glucose oxidation was preserved, but the fatty acid oxidation was significantly reduced. Insulin’s effect on substrate oxidation was significantly impaired for both the decrease in fatty acid oxidation and the increase in glucose oxidation. However, insulin-stimulated glucose uptake was normal in the infarcted hearts, consistent with normal insulin-induced phosphorylation of Akt and unchanged mRNA expression of glucose transporter type 4. The impaired oxidative response to insulin was associated with reduced mRNA expression of the genes regulating fatty acid oxidation (long-chain-acyl-coenzyme A dehydrogenase, carnitine palmitoyltransferase 1, peroxisome proliferator-activated receptor-α) and mitochondrial biogenesis (mitochondrial transcription factor A). Although mRNA expression of the mitochondrial master regulator peroxisome proliferator-activated receptor-γ coactivator 1α was normal in the infarcted hearts, the protein expression of its post-transcriptional activator, p38 mitogen-activated protein kinase, was significantly reduced. Conclusions Myocardial infarction in rats caused partial insulin resistance at the level of substrate oxidation, which was associated with mitochondrial and cardiac contractile dysfunction. Mitochondrial dysfunction was characterized by a reduced capacity to oxidize fatty acids and might have resulted from impaired mitochondrial biogenesis through the lack of p38 mitogen-activated protein kinase.</description><identifier>ISSN: 0022-5223</identifier><identifier>EISSN: 1097-685X</identifier><identifier>DOI: 10.1016/j.jtcvs.2010.08.003</identifier><identifier>PMID: 20850803</identifier><language>eng</language><publisher>United States: Mosby, Inc</publisher><subject>Acyl-CoA Dehydrogenase, Long-Chain - genetics ; Animals ; Blood Glucose - metabolism ; Cardiothoracic Surgery ; Carnitine O-Palmitoyltransferase - genetics ; Disease Models, Animal ; Fatty Acids - metabolism ; Gene Expression Regulation ; Glucose Transporter Type 4 - genetics ; Glucose Transporter Type 4 - metabolism ; Insulin - metabolism ; Insulin Resistance - genetics ; Male ; Mitochondria, Heart - metabolism ; Mitochondrial Proteins - genetics ; Mitochondrial Proteins - metabolism ; Myocardial Contraction - genetics ; Myocardial Infarction - diagnostic imaging ; Myocardial Infarction - genetics ; Myocardial Infarction - metabolism ; Myocardial Infarction - physiopathology ; Myocardium - metabolism ; Oxidation-Reduction ; p38 Mitogen-Activated Protein Kinases - metabolism ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha ; Phosphorylation ; PPAR alpha - genetics ; Proto-Oncogene Proteins c-akt - metabolism ; Rats ; Rats, Sprague-Dawley ; RNA, Messenger - metabolism ; RNA-Binding Proteins - genetics ; Time Factors ; Transcription Factors - genetics ; Ultrasonography</subject><ispartof>The Journal of thoracic and cardiovascular surgery, 2010-11, Vol.140 (5), p.1160-1167</ispartof><rights>2010</rights><rights>Copyright © 2010. Published by Mosby, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c490t-1d94d2957591b53af5c0f3245bbad05325444536eaa81af3d7c5a270e218e6ac3</citedby><cites>FETCH-LOGICAL-c490t-1d94d2957591b53af5c0f3245bbad05325444536eaa81af3d7c5a270e218e6ac3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.jtcvs.2010.08.003$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,778,782,3539,27907,27908,45978</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20850803$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Amorim, Paulo A., MD</creatorcontrib><creatorcontrib>Nguyen, T. Dung, BS</creatorcontrib><creatorcontrib>Shingu, Yasushige, MD</creatorcontrib><creatorcontrib>Schwarzer, Michael, PhD</creatorcontrib><creatorcontrib>Mohr, Friedrich W., MD, PhD</creatorcontrib><creatorcontrib>Schrepper, Andrea, MS</creatorcontrib><creatorcontrib>Doenst, Torsten, MD, PhD</creatorcontrib><title>Myocardial infarction in rats causes partial impairment in insulin response associated with reduced fatty acid oxidation and mitochondrial gene expression</title><title>The Journal of thoracic and cardiovascular surgery</title><addtitle>J Thorac Cardiovasc Surg</addtitle><description>Objective Myocardial infarction leads to contractile dysfunction. In patients with diabetes, impaired contractility has been associated with the loss of insulin effects and mitochondrial dysfunction. We assessed cardiac insulin sensitivity and mitochondrial and contractile function in rats after ligation of the left coronary artery. Methods At 2 weeks after left coronary artery ligation, we performed echocardiography in vivo and assessed the substrate use and insulin response in the isolated working heart and the regulation of insulin (Akt, glucose transporter type 4) and mitochondrial signaling (p38 mitogen-activated protein kinase, peroxisome proliferator-activated receptor-γ coactivator 1α, mitochondrial transcription factor A) using polymerase chain reaction and Western blotting. Results The infarcted hearts were dilated and had a reduced ejection fraction (ejection fraction < 50%). The basal glucose oxidation was preserved, but the fatty acid oxidation was significantly reduced. Insulin’s effect on substrate oxidation was significantly impaired for both the decrease in fatty acid oxidation and the increase in glucose oxidation. However, insulin-stimulated glucose uptake was normal in the infarcted hearts, consistent with normal insulin-induced phosphorylation of Akt and unchanged mRNA expression of glucose transporter type 4. The impaired oxidative response to insulin was associated with reduced mRNA expression of the genes regulating fatty acid oxidation (long-chain-acyl-coenzyme A dehydrogenase, carnitine palmitoyltransferase 1, peroxisome proliferator-activated receptor-α) and mitochondrial biogenesis (mitochondrial transcription factor A). Although mRNA expression of the mitochondrial master regulator peroxisome proliferator-activated receptor-γ coactivator 1α was normal in the infarcted hearts, the protein expression of its post-transcriptional activator, p38 mitogen-activated protein kinase, was significantly reduced. Conclusions Myocardial infarction in rats caused partial insulin resistance at the level of substrate oxidation, which was associated with mitochondrial and cardiac contractile dysfunction. Mitochondrial dysfunction was characterized by a reduced capacity to oxidize fatty acids and might have resulted from impaired mitochondrial biogenesis through the lack of p38 mitogen-activated protein kinase.</description><subject>Acyl-CoA Dehydrogenase, Long-Chain - genetics</subject><subject>Animals</subject><subject>Blood Glucose - metabolism</subject><subject>Cardiothoracic Surgery</subject><subject>Carnitine O-Palmitoyltransferase - genetics</subject><subject>Disease Models, Animal</subject><subject>Fatty Acids - metabolism</subject><subject>Gene Expression Regulation</subject><subject>Glucose Transporter Type 4 - genetics</subject><subject>Glucose Transporter Type 4 - metabolism</subject><subject>Insulin - metabolism</subject><subject>Insulin Resistance - genetics</subject><subject>Male</subject><subject>Mitochondria, Heart - metabolism</subject><subject>Mitochondrial Proteins - genetics</subject><subject>Mitochondrial Proteins - metabolism</subject><subject>Myocardial Contraction - genetics</subject><subject>Myocardial Infarction - diagnostic imaging</subject><subject>Myocardial Infarction - genetics</subject><subject>Myocardial Infarction - metabolism</subject><subject>Myocardial Infarction - physiopathology</subject><subject>Myocardium - metabolism</subject><subject>Oxidation-Reduction</subject><subject>p38 Mitogen-Activated Protein Kinases - metabolism</subject><subject>Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha</subject><subject>Phosphorylation</subject><subject>PPAR alpha - genetics</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>RNA, Messenger - metabolism</subject><subject>RNA-Binding Proteins - genetics</subject><subject>Time Factors</subject><subject>Transcription Factors - genetics</subject><subject>Ultrasonography</subject><issn>0022-5223</issn><issn>1097-685X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFks1u1DAUhSMEokPhCZBQdqxmem3H-VmAhKoClYpYAFJ31h37hnpI7GA7pfMqPC3OTGHBpiv_ffdc65xbFC8ZbBiw-my32SV9Gzcc8g20GwDxqFgx6Jp13crrx8UKgPO15FycFM9i3AFAA6x7WpxwaCW0IFbF7097rzEYi0NpXY9BJ-td3pYBUyw1zpFiOWFIB2Kc0IaRXFoI6-I8LCTFybtIJcbotcVEpvxl001-MLPOhx5T2peorSn9nTV4aIHOlKNNXt94Z8Ki_p0clXQ3Zb2YiefFkx6HSC_u19Pi2_uLr-cf11efP1yev7ta66qDtGamqwzvZCM7tpUCe6mhF7yS2y0akILLqqqkqAmxZdgL02iJvAHirKUatTgtXh91p-B_zhSTGm3UNAzoyM9RdbKqgTWyfpBcviCgangmxZHUwccYqFdTsCOGvWKglvTUTh3SU0t6ClqV08tVr-715-1I5l_N37gy8OYIUPbj1lJQUVty2WMbSCdlvH2gwdv_6nUO0GocftCe4s7PwWWrFVORK1BflgFa5ofl0Wnr7lr8ARc3xTQ</recordid><startdate>20101101</startdate><enddate>20101101</enddate><creator>Amorim, Paulo A., MD</creator><creator>Nguyen, T. Dung, BS</creator><creator>Shingu, Yasushige, MD</creator><creator>Schwarzer, Michael, PhD</creator><creator>Mohr, Friedrich W., MD, PhD</creator><creator>Schrepper, Andrea, MS</creator><creator>Doenst, Torsten, MD, PhD</creator><general>Mosby, Inc</general><scope>6I.</scope><scope>AAFTH</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><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>20101101</creationdate><title>Myocardial infarction in rats causes partial impairment in insulin response associated with reduced fatty acid oxidation and mitochondrial gene expression</title><author>Amorim, Paulo A., MD ; Nguyen, T. Dung, BS ; Shingu, Yasushige, MD ; Schwarzer, Michael, PhD ; Mohr, Friedrich W., MD, PhD ; Schrepper, Andrea, MS ; Doenst, Torsten, MD, PhD</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c490t-1d94d2957591b53af5c0f3245bbad05325444536eaa81af3d7c5a270e218e6ac3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Acyl-CoA Dehydrogenase, Long-Chain - genetics</topic><topic>Animals</topic><topic>Blood Glucose - metabolism</topic><topic>Cardiothoracic Surgery</topic><topic>Carnitine O-Palmitoyltransferase - genetics</topic><topic>Disease Models, Animal</topic><topic>Fatty Acids - metabolism</topic><topic>Gene Expression Regulation</topic><topic>Glucose Transporter Type 4 - genetics</topic><topic>Glucose Transporter Type 4 - metabolism</topic><topic>Insulin - metabolism</topic><topic>Insulin Resistance - genetics</topic><topic>Male</topic><topic>Mitochondria, Heart - metabolism</topic><topic>Mitochondrial Proteins - genetics</topic><topic>Mitochondrial Proteins - metabolism</topic><topic>Myocardial Contraction - genetics</topic><topic>Myocardial Infarction - diagnostic imaging</topic><topic>Myocardial Infarction - genetics</topic><topic>Myocardial Infarction - metabolism</topic><topic>Myocardial Infarction - physiopathology</topic><topic>Myocardium - metabolism</topic><topic>Oxidation-Reduction</topic><topic>p38 Mitogen-Activated Protein Kinases - metabolism</topic><topic>Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha</topic><topic>Phosphorylation</topic><topic>PPAR alpha - genetics</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>RNA, Messenger - metabolism</topic><topic>RNA-Binding Proteins - genetics</topic><topic>Time Factors</topic><topic>Transcription Factors - genetics</topic><topic>Ultrasonography</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Amorim, Paulo A., MD</creatorcontrib><creatorcontrib>Nguyen, T. Dung, BS</creatorcontrib><creatorcontrib>Shingu, Yasushige, MD</creatorcontrib><creatorcontrib>Schwarzer, Michael, PhD</creatorcontrib><creatorcontrib>Mohr, Friedrich W., MD, PhD</creatorcontrib><creatorcontrib>Schrepper, Andrea, MS</creatorcontrib><creatorcontrib>Doenst, Torsten, MD, PhD</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</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><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>The Journal of thoracic and cardiovascular surgery</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Amorim, Paulo A., MD</au><au>Nguyen, T. Dung, BS</au><au>Shingu, Yasushige, MD</au><au>Schwarzer, Michael, PhD</au><au>Mohr, Friedrich W., MD, PhD</au><au>Schrepper, Andrea, MS</au><au>Doenst, Torsten, MD, PhD</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Myocardial infarction in rats causes partial impairment in insulin response associated with reduced fatty acid oxidation and mitochondrial gene expression</atitle><jtitle>The Journal of thoracic and cardiovascular surgery</jtitle><addtitle>J Thorac Cardiovasc Surg</addtitle><date>2010-11-01</date><risdate>2010</risdate><volume>140</volume><issue>5</issue><spage>1160</spage><epage>1167</epage><pages>1160-1167</pages><issn>0022-5223</issn><eissn>1097-685X</eissn><abstract>Objective Myocardial infarction leads to contractile dysfunction. In patients with diabetes, impaired contractility has been associated with the loss of insulin effects and mitochondrial dysfunction. We assessed cardiac insulin sensitivity and mitochondrial and contractile function in rats after ligation of the left coronary artery. Methods At 2 weeks after left coronary artery ligation, we performed echocardiography in vivo and assessed the substrate use and insulin response in the isolated working heart and the regulation of insulin (Akt, glucose transporter type 4) and mitochondrial signaling (p38 mitogen-activated protein kinase, peroxisome proliferator-activated receptor-γ coactivator 1α, mitochondrial transcription factor A) using polymerase chain reaction and Western blotting. Results The infarcted hearts were dilated and had a reduced ejection fraction (ejection fraction < 50%). The basal glucose oxidation was preserved, but the fatty acid oxidation was significantly reduced. Insulin’s effect on substrate oxidation was significantly impaired for both the decrease in fatty acid oxidation and the increase in glucose oxidation. However, insulin-stimulated glucose uptake was normal in the infarcted hearts, consistent with normal insulin-induced phosphorylation of Akt and unchanged mRNA expression of glucose transporter type 4. The impaired oxidative response to insulin was associated with reduced mRNA expression of the genes regulating fatty acid oxidation (long-chain-acyl-coenzyme A dehydrogenase, carnitine palmitoyltransferase 1, peroxisome proliferator-activated receptor-α) and mitochondrial biogenesis (mitochondrial transcription factor A). Although mRNA expression of the mitochondrial master regulator peroxisome proliferator-activated receptor-γ coactivator 1α was normal in the infarcted hearts, the protein expression of its post-transcriptional activator, p38 mitogen-activated protein kinase, was significantly reduced. Conclusions Myocardial infarction in rats caused partial insulin resistance at the level of substrate oxidation, which was associated with mitochondrial and cardiac contractile dysfunction. Mitochondrial dysfunction was characterized by a reduced capacity to oxidize fatty acids and might have resulted from impaired mitochondrial biogenesis through the lack of p38 mitogen-activated protein kinase.</abstract><cop>United States</cop><pub>Mosby, Inc</pub><pmid>20850803</pmid><doi>10.1016/j.jtcvs.2010.08.003</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Acyl-CoA Dehydrogenase, Long-Chain - genetics Animals Blood Glucose - metabolism Cardiothoracic Surgery Carnitine O-Palmitoyltransferase - genetics Disease Models, Animal Fatty Acids - metabolism Gene Expression Regulation Glucose Transporter Type 4 - genetics Glucose Transporter Type 4 - metabolism Insulin - metabolism Insulin Resistance - genetics Male Mitochondria, Heart - metabolism Mitochondrial Proteins - genetics Mitochondrial Proteins - metabolism Myocardial Contraction - genetics Myocardial Infarction - diagnostic imaging Myocardial Infarction - genetics Myocardial Infarction - metabolism Myocardial Infarction - physiopathology Myocardium - metabolism Oxidation-Reduction p38 Mitogen-Activated Protein Kinases - metabolism Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha Phosphorylation PPAR alpha - genetics Proto-Oncogene Proteins c-akt - metabolism Rats Rats, Sprague-Dawley RNA, Messenger - metabolism RNA-Binding Proteins - genetics Time Factors Transcription Factors - genetics Ultrasonography |
| title | Myocardial infarction in rats causes partial impairment in insulin response associated with reduced fatty acid oxidation and mitochondrial gene expression |
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