Mitochondrial biogenesis and PGC‐1α gene expression in male broilers from ascites‐susceptible and ‐resistant lines
Summary Ascites is a cardiovascular metabolic disease characterized by accumulation of fluid around the heart and in the abdominal cavity that eventually leads to death. This syndrome is the end‐point result of a series of metabolic incidents that are generally caused by impaired oxygen availability...
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Veröffentlicht in: | Journal of animal physiology and animal nutrition 2018-02, Vol.102 (1), p.e482-e485 |
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creator | Khodambashi Emami, N. Golian, A. Danesh Mesgaran, M. Anthony, N. B. Rhoads, D. D. |
description | Summary
Ascites is a cardiovascular metabolic disease characterized by accumulation of fluid around the heart and in the abdominal cavity that eventually leads to death. This syndrome is the end‐point result of a series of metabolic incidents that are generally caused by impaired oxygen availability. Mitochondria are the major sites of oxygen consumption, therefore major contributors to oxidative stress. Genetic, metabolic and dietary factors can influence variations in mitochondrial biogenesis (mitochondrial size, number and mass) that might have an effect on oxygen consumption and reactive oxygen species production. This study evaluated the effect of genotype on PGC‐1α mRNA gene expression and mitochondrial biogenesis. These parameters were examined in male broiler chickens at 22 weeks of age from the SUS and RES lines divergently selected for ascites phenotype. From each line, five birds were sampled for right ventricle and breast muscle. Gene expression and mtDNA copy number were assessed by quantitative PCR. Results showed that birds from SUS had significantly higher PGC‐1α mRNA gene (p = .033) and mitochondrial DNA copy number (p = .038) in breast muscle. There was no difference in right ventricle PGC‐1α expression or mitochondrial DNA copy number between the two lines. These findings indicate that mitochondrial biogenesis and PGC‐1α mRNA gene expression differ between male broiler chickens from RES and SUS lines in a tissue‐specific manner. |
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Ascites is a cardiovascular metabolic disease characterized by accumulation of fluid around the heart and in the abdominal cavity that eventually leads to death. This syndrome is the end‐point result of a series of metabolic incidents that are generally caused by impaired oxygen availability. Mitochondria are the major sites of oxygen consumption, therefore major contributors to oxidative stress. Genetic, metabolic and dietary factors can influence variations in mitochondrial biogenesis (mitochondrial size, number and mass) that might have an effect on oxygen consumption and reactive oxygen species production. This study evaluated the effect of genotype on PGC‐1α mRNA gene expression and mitochondrial biogenesis. These parameters were examined in male broiler chickens at 22 weeks of age from the SUS and RES lines divergently selected for ascites phenotype. From each line, five birds were sampled for right ventricle and breast muscle. Gene expression and mtDNA copy number were assessed by quantitative PCR. Results showed that birds from SUS had significantly higher PGC‐1α mRNA gene (p = .033) and mitochondrial DNA copy number (p = .038) in breast muscle. There was no difference in right ventricle PGC‐1α expression or mitochondrial DNA copy number between the two lines. These findings indicate that mitochondrial biogenesis and PGC‐1α mRNA gene expression differ between male broiler chickens from RES and SUS lines in a tissue‐specific manner.</description><identifier>ISSN: 0931-2439</identifier><identifier>EISSN: 1439-0396</identifier><identifier>DOI: 10.1111/jpn.12706</identifier><identifier>PMID: 28439972</identifier><language>eng</language><publisher>Germany</publisher><subject>abdominal cavity ; Animals ; ascites ; Ascites - genetics ; Ascites - veterinary ; biogenesis ; breast muscle ; broiler chickens ; broilers ; Chickens - genetics ; death ; diet ; gene expression ; Gene Expression Regulation ; genes ; genotype ; heart ; Male ; males ; messenger RNA ; metabolic diseases ; mitochondria ; Mitochondria - physiology ; mitochondrial DNA ; Organelle Biogenesis ; oxidative stress ; oxygen ; oxygen consumption ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - genetics ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - metabolism ; PGC‐1α ; phenotype ; Polymerase Chain Reaction ; Poultry Diseases - genetics ; quantitative polymerase chain reaction ; reactive oxygen species ; RNA, Messenger - genetics ; RNA, Messenger - metabolism</subject><ispartof>Journal of animal physiology and animal nutrition, 2018-02, Vol.102 (1), p.e482-e485</ispartof><rights>2017 Blackwell Verlag GmbH</rights><rights>2017 Blackwell Verlag GmbH.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3586-3d35acbe3a8174fc9bc9d78690e78682e35b5b4f7287fb57d530874067419e3a3</citedby><cites>FETCH-LOGICAL-c3586-3d35acbe3a8174fc9bc9d78690e78682e35b5b4f7287fb57d530874067419e3a3</cites><orcidid>0000-0003-3657-7728</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fjpn.12706$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fjpn.12706$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,777,781,1412,27905,27906,45555,45556</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28439972$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Khodambashi Emami, N.</creatorcontrib><creatorcontrib>Golian, A.</creatorcontrib><creatorcontrib>Danesh Mesgaran, M.</creatorcontrib><creatorcontrib>Anthony, N. B.</creatorcontrib><creatorcontrib>Rhoads, D. D.</creatorcontrib><title>Mitochondrial biogenesis and PGC‐1α gene expression in male broilers from ascites‐susceptible and ‐resistant lines</title><title>Journal of animal physiology and animal nutrition</title><addtitle>J Anim Physiol Anim Nutr (Berl)</addtitle><description>Summary
Ascites is a cardiovascular metabolic disease characterized by accumulation of fluid around the heart and in the abdominal cavity that eventually leads to death. This syndrome is the end‐point result of a series of metabolic incidents that are generally caused by impaired oxygen availability. Mitochondria are the major sites of oxygen consumption, therefore major contributors to oxidative stress. Genetic, metabolic and dietary factors can influence variations in mitochondrial biogenesis (mitochondrial size, number and mass) that might have an effect on oxygen consumption and reactive oxygen species production. This study evaluated the effect of genotype on PGC‐1α mRNA gene expression and mitochondrial biogenesis. These parameters were examined in male broiler chickens at 22 weeks of age from the SUS and RES lines divergently selected for ascites phenotype. From each line, five birds were sampled for right ventricle and breast muscle. Gene expression and mtDNA copy number were assessed by quantitative PCR. Results showed that birds from SUS had significantly higher PGC‐1α mRNA gene (p = .033) and mitochondrial DNA copy number (p = .038) in breast muscle. There was no difference in right ventricle PGC‐1α expression or mitochondrial DNA copy number between the two lines. These findings indicate that mitochondrial biogenesis and PGC‐1α mRNA gene expression differ between male broiler chickens from RES and SUS lines in a tissue‐specific manner.</description><subject>abdominal cavity</subject><subject>Animals</subject><subject>ascites</subject><subject>Ascites - genetics</subject><subject>Ascites - veterinary</subject><subject>biogenesis</subject><subject>breast muscle</subject><subject>broiler chickens</subject><subject>broilers</subject><subject>Chickens - genetics</subject><subject>death</subject><subject>diet</subject><subject>gene expression</subject><subject>Gene Expression Regulation</subject><subject>genes</subject><subject>genotype</subject><subject>heart</subject><subject>Male</subject><subject>males</subject><subject>messenger RNA</subject><subject>metabolic diseases</subject><subject>mitochondria</subject><subject>Mitochondria - physiology</subject><subject>mitochondrial DNA</subject><subject>Organelle Biogenesis</subject><subject>oxidative stress</subject><subject>oxygen</subject><subject>oxygen consumption</subject><subject>Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - genetics</subject><subject>Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - metabolism</subject><subject>PGC‐1α</subject><subject>phenotype</subject><subject>Polymerase Chain Reaction</subject><subject>Poultry Diseases - genetics</subject><subject>quantitative polymerase chain reaction</subject><subject>reactive oxygen species</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><issn>0931-2439</issn><issn>1439-0396</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU1OxCAYhonR6Di68AKGpS7qQCmlLM1ER41_C1030FJl0pYKnejsPIJX8SIewpP4jTO6MxICyZuHB8KL0B4lRxTGaNq1RzQWJF1DA5owGREm03U0IJLRKIZgC22HMCWECk7STbQVZxBKEQ_Q_Mr2rnh0bemtqrG27sG0JtiAVVvi28n48_WNfrzjRYrNS-dNCNa12La4UbXB2jtbGx9w5V2DVShsbwKcCbNQmK63GpiFCSK_0Paq7XFt4YodtFGpOpjd1T5E96cnd-Oz6PJmcj4-vowKxrM0YiXjqtCGqYyKpCqkLmQpslQSA2sWG8Y110kl4kxUmouSM5KJhKQioRJOsSE6WHo7755mJvR5Y-Ftda1a42YhjwGNecoT-S9KMwmTpJICerhEC-9C8KbKO28b5ec5JfmilBxKyb9LAXZ_pZ3pxpS_5E8LAIyWwDP85fxvU35xe71UfgG2A5p7</recordid><startdate>201802</startdate><enddate>201802</enddate><creator>Khodambashi Emami, N.</creator><creator>Golian, A.</creator><creator>Danesh Mesgaran, M.</creator><creator>Anthony, N. B.</creator><creator>Rhoads, D. D.</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><scope>7S9</scope><scope>L.6</scope><orcidid>https://orcid.org/0000-0003-3657-7728</orcidid></search><sort><creationdate>201802</creationdate><title>Mitochondrial biogenesis and PGC‐1α gene expression in male broilers from ascites‐susceptible and ‐resistant lines</title><author>Khodambashi Emami, N. ; Golian, A. ; Danesh Mesgaran, M. ; Anthony, N. B. ; Rhoads, D. D.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3586-3d35acbe3a8174fc9bc9d78690e78682e35b5b4f7287fb57d530874067419e3a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>abdominal cavity</topic><topic>Animals</topic><topic>ascites</topic><topic>Ascites - genetics</topic><topic>Ascites - veterinary</topic><topic>biogenesis</topic><topic>breast muscle</topic><topic>broiler chickens</topic><topic>broilers</topic><topic>Chickens - genetics</topic><topic>death</topic><topic>diet</topic><topic>gene expression</topic><topic>Gene Expression Regulation</topic><topic>genes</topic><topic>genotype</topic><topic>heart</topic><topic>Male</topic><topic>males</topic><topic>messenger RNA</topic><topic>metabolic diseases</topic><topic>mitochondria</topic><topic>Mitochondria - physiology</topic><topic>mitochondrial DNA</topic><topic>Organelle Biogenesis</topic><topic>oxidative stress</topic><topic>oxygen</topic><topic>oxygen consumption</topic><topic>Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - genetics</topic><topic>Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - metabolism</topic><topic>PGC‐1α</topic><topic>phenotype</topic><topic>Polymerase Chain Reaction</topic><topic>Poultry Diseases - genetics</topic><topic>quantitative polymerase chain reaction</topic><topic>reactive oxygen species</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Khodambashi Emami, N.</creatorcontrib><creatorcontrib>Golian, A.</creatorcontrib><creatorcontrib>Danesh Mesgaran, M.</creatorcontrib><creatorcontrib>Anthony, N. B.</creatorcontrib><creatorcontrib>Rhoads, D. D.</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><collection>AGRICOLA</collection><collection>AGRICOLA - Academic</collection><jtitle>Journal of animal physiology and animal nutrition</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Khodambashi Emami, N.</au><au>Golian, A.</au><au>Danesh Mesgaran, M.</au><au>Anthony, N. B.</au><au>Rhoads, D. D.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mitochondrial biogenesis and PGC‐1α gene expression in male broilers from ascites‐susceptible and ‐resistant lines</atitle><jtitle>Journal of animal physiology and animal nutrition</jtitle><addtitle>J Anim Physiol Anim Nutr (Berl)</addtitle><date>2018-02</date><risdate>2018</risdate><volume>102</volume><issue>1</issue><spage>e482</spage><epage>e485</epage><pages>e482-e485</pages><issn>0931-2439</issn><eissn>1439-0396</eissn><abstract>Summary
Ascites is a cardiovascular metabolic disease characterized by accumulation of fluid around the heart and in the abdominal cavity that eventually leads to death. This syndrome is the end‐point result of a series of metabolic incidents that are generally caused by impaired oxygen availability. Mitochondria are the major sites of oxygen consumption, therefore major contributors to oxidative stress. Genetic, metabolic and dietary factors can influence variations in mitochondrial biogenesis (mitochondrial size, number and mass) that might have an effect on oxygen consumption and reactive oxygen species production. This study evaluated the effect of genotype on PGC‐1α mRNA gene expression and mitochondrial biogenesis. These parameters were examined in male broiler chickens at 22 weeks of age from the SUS and RES lines divergently selected for ascites phenotype. From each line, five birds were sampled for right ventricle and breast muscle. Gene expression and mtDNA copy number were assessed by quantitative PCR. Results showed that birds from SUS had significantly higher PGC‐1α mRNA gene (p = .033) and mitochondrial DNA copy number (p = .038) in breast muscle. There was no difference in right ventricle PGC‐1α expression or mitochondrial DNA copy number between the two lines. These findings indicate that mitochondrial biogenesis and PGC‐1α mRNA gene expression differ between male broiler chickens from RES and SUS lines in a tissue‐specific manner.</abstract><cop>Germany</cop><pmid>28439972</pmid><doi>10.1111/jpn.12706</doi><tpages>4</tpages><orcidid>https://orcid.org/0000-0003-3657-7728</orcidid></addata></record> |
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subjects | abdominal cavity Animals ascites Ascites - genetics Ascites - veterinary biogenesis breast muscle broiler chickens broilers Chickens - genetics death diet gene expression Gene Expression Regulation genes genotype heart Male males messenger RNA metabolic diseases mitochondria Mitochondria - physiology mitochondrial DNA Organelle Biogenesis oxidative stress oxygen oxygen consumption Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - genetics Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - metabolism PGC‐1α phenotype Polymerase Chain Reaction Poultry Diseases - genetics quantitative polymerase chain reaction reactive oxygen species RNA, Messenger - genetics RNA, Messenger - metabolism |
title | Mitochondrial biogenesis and PGC‐1α gene expression in male broilers from ascites‐susceptible and ‐resistant lines |
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