Isolation of a Genomic Region Affecting Most Components of Metabolic Syndrome in a Chromosome-16 Congenic Rat Model
Metabolic syndrome is a highly prevalent human disease with substantial genomic and environmental components. Previous studies indicate the presence of significant genetic determinants of several features of metabolic syndrome on rat chromosome 16 (RNO16) and the syntenic regions of human genome. We...
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| Veröffentlicht in: | PloS one 2016-03, Vol.11 (3), p.e0152708-e0152708 |
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| creator | Šedová, Lucie Pravenec, Michal Křenová, Drahomíra Kazdová, Ludmila Zídek, Václav Krupková, Michaela Liška, František Křen, Vladimír Šeda, Ondřej |
| description | Metabolic syndrome is a highly prevalent human disease with substantial genomic and environmental components. Previous studies indicate the presence of significant genetic determinants of several features of metabolic syndrome on rat chromosome 16 (RNO16) and the syntenic regions of human genome. We derived the SHR.BN16 congenic strain by introgression of a limited RNO16 region from the Brown Norway congenic strain (BN-Lx) into the genomic background of the spontaneously hypertensive rat (SHR) strain. We compared the morphometric, metabolic, and hemodynamic profiles of adult male SHR and SHR.BN16 rats. We also compared in silico the DNA sequences for the differential segment in the BN-Lx and SHR parental strains. SHR.BN16 congenic rats had significantly lower weight, decreased concentrations of total triglycerides and cholesterol, and improved glucose tolerance compared with SHR rats. The concentrations of insulin, free fatty acids, and adiponectin were comparable between the two strains. SHR.BN16 rats had significantly lower systolic (18-28 mmHg difference) and diastolic (10-15 mmHg difference) blood pressure throughout the experiment (repeated-measures ANOVA, P < 0.001). The differential segment spans approximately 22 Mb of the telomeric part of the short arm of RNO16. The in silico analyses revealed over 1200 DNA variants between the BN-Lx and SHR genomes in the SHR.BN16 differential segment, 44 of which lead to missense mutations, and only eight of which (in Asb14, Il17rd, Itih1, Syt15, Ercc6, RGD1564958, Tmem161a, and Gatad2a genes) are predicted to be damaging to the protein product. Furthermore, a number of genes within the RNO16 differential segment associated with metabolic syndrome components in human studies showed polymorphisms between SHR and BN-Lx (including Lpl, Nrg3, Pbx4, Cilp2, and Stab1). Our novel congenic rat model demonstrates that a limited genomic region on RNO16 in the SHR significantly affects many of the features of metabolic syndrome. |
| doi_str_mv | 10.1371/journal.pone.0152708 |
| format | Article |
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Previous studies indicate the presence of significant genetic determinants of several features of metabolic syndrome on rat chromosome 16 (RNO16) and the syntenic regions of human genome. We derived the SHR.BN16 congenic strain by introgression of a limited RNO16 region from the Brown Norway congenic strain (BN-Lx) into the genomic background of the spontaneously hypertensive rat (SHR) strain. We compared the morphometric, metabolic, and hemodynamic profiles of adult male SHR and SHR.BN16 rats. We also compared in silico the DNA sequences for the differential segment in the BN-Lx and SHR parental strains. SHR.BN16 congenic rats had significantly lower weight, decreased concentrations of total triglycerides and cholesterol, and improved glucose tolerance compared with SHR rats. The concentrations of insulin, free fatty acids, and adiponectin were comparable between the two strains. SHR.BN16 rats had significantly lower systolic (18-28 mmHg difference) and diastolic (10-15 mmHg difference) blood pressure throughout the experiment (repeated-measures ANOVA, P < 0.001). The differential segment spans approximately 22 Mb of the telomeric part of the short arm of RNO16. The in silico analyses revealed over 1200 DNA variants between the BN-Lx and SHR genomes in the SHR.BN16 differential segment, 44 of which lead to missense mutations, and only eight of which (in Asb14, Il17rd, Itih1, Syt15, Ercc6, RGD1564958, Tmem161a, and Gatad2a genes) are predicted to be damaging to the protein product. Furthermore, a number of genes within the RNO16 differential segment associated with metabolic syndrome components in human studies showed polymorphisms between SHR and BN-Lx (including Lpl, Nrg3, Pbx4, Cilp2, and Stab1). Our novel congenic rat model demonstrates that a limited genomic region on RNO16 in the SHR significantly affects many of the features of metabolic syndrome.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0152708</identifier><identifier>PMID: 27031336</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adiponectin ; Animals ; Animals, Congenic - genetics ; Animals, Congenic - metabolism ; Animals, Congenic - physiology ; Biology ; Biology and Life Sciences ; Blood pressure ; Cholesterol ; Chromosome 16 ; Chromosomes ; Chromosomes, Human, Pair 16 - genetics ; Comparative analysis ; Deoxyribonucleic acid ; Diabetes ; DNA ; Fatty acids ; Gene expression ; Gene sequencing ; Genes ; Genetic aspects ; Genetic polymorphisms ; Genetics ; Genome ; Genomes ; Genomics ; Glucose tolerance ; Glucose Tolerance Test ; Hemodynamics ; Humans ; Hypertension ; Insulin ; Insulin resistance ; Interleukin 1 ; Male ; Medicine ; Medicine and Health Sciences ; Metabolic syndrome ; Metabolic Syndrome - genetics ; Metabolic Syndrome - metabolism ; Metabolic Syndrome - physiopathology ; Metabolic syndrome X ; Metabolome ; Missense mutation ; Mutation ; Nucleotide sequence ; Physiological aspects ; Physiology ; Rats ; Rats, Inbred BN - genetics ; Rats, Inbred BN - metabolism ; Rats, Inbred BN - physiology ; Rats, Inbred SHR - genetics ; Rats, Inbred SHR - metabolism ; Rats, Inbred SHR - physiology ; Research and Analysis Methods ; Risk factors ; Rodents ; Studies ; Synteny ; Triglycerides ; Variance analysis</subject><ispartof>PloS one, 2016-03, Vol.11 (3), p.e0152708-e0152708</ispartof><rights>COPYRIGHT 2016 Public Library of Science</rights><rights>2016 Šedová et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2016 Šedová et al 2016 Šedová et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c725t-3d3219b05ab35725df5bdf49cb959914cabde3112e965f250e06205e8229ecd63</citedby><cites>FETCH-LOGICAL-c725t-3d3219b05ab35725df5bdf49cb959914cabde3112e965f250e06205e8229ecd63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4816345/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4816345/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,865,886,2103,2929,23871,27929,27930,53796,53798</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27031336$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Alemany, Marià</contributor><creatorcontrib>Šedová, Lucie</creatorcontrib><creatorcontrib>Pravenec, Michal</creatorcontrib><creatorcontrib>Křenová, Drahomíra</creatorcontrib><creatorcontrib>Kazdová, Ludmila</creatorcontrib><creatorcontrib>Zídek, Václav</creatorcontrib><creatorcontrib>Krupková, Michaela</creatorcontrib><creatorcontrib>Liška, František</creatorcontrib><creatorcontrib>Křen, Vladimír</creatorcontrib><creatorcontrib>Šeda, Ondřej</creatorcontrib><title>Isolation of a Genomic Region Affecting Most Components of Metabolic Syndrome in a Chromosome-16 Congenic Rat Model</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Metabolic syndrome is a highly prevalent human disease with substantial genomic and environmental components. Previous studies indicate the presence of significant genetic determinants of several features of metabolic syndrome on rat chromosome 16 (RNO16) and the syntenic regions of human genome. We derived the SHR.BN16 congenic strain by introgression of a limited RNO16 region from the Brown Norway congenic strain (BN-Lx) into the genomic background of the spontaneously hypertensive rat (SHR) strain. We compared the morphometric, metabolic, and hemodynamic profiles of adult male SHR and SHR.BN16 rats. We also compared in silico the DNA sequences for the differential segment in the BN-Lx and SHR parental strains. SHR.BN16 congenic rats had significantly lower weight, decreased concentrations of total triglycerides and cholesterol, and improved glucose tolerance compared with SHR rats. The concentrations of insulin, free fatty acids, and adiponectin were comparable between the two strains. SHR.BN16 rats had significantly lower systolic (18-28 mmHg difference) and diastolic (10-15 mmHg difference) blood pressure throughout the experiment (repeated-measures ANOVA, P < 0.001). The differential segment spans approximately 22 Mb of the telomeric part of the short arm of RNO16. The in silico analyses revealed over 1200 DNA variants between the BN-Lx and SHR genomes in the SHR.BN16 differential segment, 44 of which lead to missense mutations, and only eight of which (in Asb14, Il17rd, Itih1, Syt15, Ercc6, RGD1564958, Tmem161a, and Gatad2a genes) are predicted to be damaging to the protein product. Furthermore, a number of genes within the RNO16 differential segment associated with metabolic syndrome components in human studies showed polymorphisms between SHR and BN-Lx (including Lpl, Nrg3, Pbx4, Cilp2, and Stab1). Our novel congenic rat model demonstrates that a limited genomic region on RNO16 in the SHR significantly affects many of the features of metabolic syndrome.</description><subject>Adiponectin</subject><subject>Animals</subject><subject>Animals, Congenic - genetics</subject><subject>Animals, Congenic - metabolism</subject><subject>Animals, Congenic - physiology</subject><subject>Biology</subject><subject>Biology and Life Sciences</subject><subject>Blood pressure</subject><subject>Cholesterol</subject><subject>Chromosome 16</subject><subject>Chromosomes</subject><subject>Chromosomes, Human, Pair 16 - genetics</subject><subject>Comparative analysis</subject><subject>Deoxyribonucleic acid</subject><subject>Diabetes</subject><subject>DNA</subject><subject>Fatty acids</subject><subject>Gene expression</subject><subject>Gene sequencing</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Genetic polymorphisms</subject><subject>Genetics</subject><subject>Genome</subject><subject>Genomes</subject><subject>Genomics</subject><subject>Glucose tolerance</subject><subject>Glucose Tolerance Test</subject><subject>Hemodynamics</subject><subject>Humans</subject><subject>Hypertension</subject><subject>Insulin</subject><subject>Insulin resistance</subject><subject>Interleukin 1</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine and Health Sciences</subject><subject>Metabolic syndrome</subject><subject>Metabolic Syndrome - genetics</subject><subject>Metabolic Syndrome - metabolism</subject><subject>Metabolic Syndrome - physiopathology</subject><subject>Metabolic syndrome X</subject><subject>Metabolome</subject><subject>Missense mutation</subject><subject>Mutation</subject><subject>Nucleotide sequence</subject><subject>Physiological aspects</subject><subject>Physiology</subject><subject>Rats</subject><subject>Rats, Inbred BN - genetics</subject><subject>Rats, Inbred BN - metabolism</subject><subject>Rats, Inbred BN - physiology</subject><subject>Rats, Inbred SHR - genetics</subject><subject>Rats, Inbred SHR - metabolism</subject><subject>Rats, Inbred SHR - physiology</subject><subject>Research and Analysis Methods</subject><subject>Risk factors</subject><subject>Rodents</subject><subject>Studies</subject><subject>Synteny</subject><subject>Triglycerides</subject><subject>Variance analysis</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNk1GL1DAQx4so3nn6DUQLgujDrknTNM2LsCx6LtxxcKe-hjSddru0ydqk4n17p27v2MqB0oem09_8M_lnJopeUrKkTNAPOzf0VrfLvbOwJJQnguSPolMqWbLIEsIeH61Pomfe7wjhLM-yp9EJsowylp1GfuNdq0PjbOyqWMfnYF3XmPga6jG2qiowobF1fOl8iNeuG7ezwY_0JQRduBbpm1tb9q6DuLGosd7i2nn8XtAMc2wNdpTUAVVKaJ9HTyrdengxvc-ib58_fV1_WVxcnW_Wq4uFEQkPC1ayhMqCcF0wjpGy4kVZpdIUkktJU6OLEhilCciMVwknQPCsHPIkkWDKjJ1Frw-6-9Z5NfnlFRVCcJaSlCKxORCl0zu175tO97fK6Ub9Cbi-VroPjWlBocOi1IJyymVKIcshlQkrtCQMKiEMan2cdhuKDkqDLvW6nYnO_9hmq2r3U6U5zVjKUeDdJNC7HwP4oLrGG2hbbcENWHdOeCpzKti_USFyQST6geibv9CHjZioWuNZG1s5LNGMomqFpaWcilwitXyAwqcE7BlsjKrB-Czh_SwBmQC_Qq0H79Xm5vr_2avvc_btEbsF3YYt9vEw9rGfg-kBNL3zvofq_j4oUeMY3bmhxr5W0xhh2qvju7xPupsb9hs_GBVp</recordid><startdate>20160331</startdate><enddate>20160331</enddate><creator>Šedová, Lucie</creator><creator>Pravenec, Michal</creator><creator>Křenová, Drahomíra</creator><creator>Kazdová, Ludmila</creator><creator>Zídek, Václav</creator><creator>Krupková, Michaela</creator><creator>Liška, František</creator><creator>Křen, Vladimír</creator><creator>Šeda, Ondřej</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20160331</creationdate><title>Isolation of a Genomic Region Affecting Most Components of Metabolic Syndrome in a Chromosome-16 Congenic Rat Model</title><author>Šedová, Lucie ; Pravenec, Michal ; Křenová, Drahomíra ; Kazdová, Ludmila ; Zídek, Václav ; Krupková, Michaela ; Liška, František ; Křen, Vladimír ; Šeda, Ondřej</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c725t-3d3219b05ab35725df5bdf49cb959914cabde3112e965f250e06205e8229ecd63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Adiponectin</topic><topic>Animals</topic><topic>Animals, Congenic - genetics</topic><topic>Animals, Congenic - metabolism</topic><topic>Animals, Congenic - physiology</topic><topic>Biology</topic><topic>Biology and Life Sciences</topic><topic>Blood pressure</topic><topic>Cholesterol</topic><topic>Chromosome 16</topic><topic>Chromosomes</topic><topic>Chromosomes, Human, Pair 16 - genetics</topic><topic>Comparative analysis</topic><topic>Deoxyribonucleic acid</topic><topic>Diabetes</topic><topic>DNA</topic><topic>Fatty acids</topic><topic>Gene expression</topic><topic>Gene sequencing</topic><topic>Genes</topic><topic>Genetic aspects</topic><topic>Genetic polymorphisms</topic><topic>Genetics</topic><topic>Genome</topic><topic>Genomes</topic><topic>Genomics</topic><topic>Glucose tolerance</topic><topic>Glucose Tolerance Test</topic><topic>Hemodynamics</topic><topic>Humans</topic><topic>Hypertension</topic><topic>Insulin</topic><topic>Insulin resistance</topic><topic>Interleukin 1</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine and Health Sciences</topic><topic>Metabolic syndrome</topic><topic>Metabolic Syndrome - 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Academic</collection><collection>ProQuest Engineering Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Engineering Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Materials Science Collection</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Šedová, Lucie</au><au>Pravenec, Michal</au><au>Křenová, Drahomíra</au><au>Kazdová, Ludmila</au><au>Zídek, Václav</au><au>Krupková, Michaela</au><au>Liška, František</au><au>Křen, Vladimír</au><au>Šeda, Ondřej</au><au>Alemany, Marià</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Isolation of a Genomic Region Affecting Most Components of Metabolic Syndrome in a Chromosome-16 Congenic Rat Model</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2016-03-31</date><risdate>2016</risdate><volume>11</volume><issue>3</issue><spage>e0152708</spage><epage>e0152708</epage><pages>e0152708-e0152708</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Metabolic syndrome is a highly prevalent human disease with substantial genomic and environmental components. Previous studies indicate the presence of significant genetic determinants of several features of metabolic syndrome on rat chromosome 16 (RNO16) and the syntenic regions of human genome. We derived the SHR.BN16 congenic strain by introgression of a limited RNO16 region from the Brown Norway congenic strain (BN-Lx) into the genomic background of the spontaneously hypertensive rat (SHR) strain. We compared the morphometric, metabolic, and hemodynamic profiles of adult male SHR and SHR.BN16 rats. We also compared in silico the DNA sequences for the differential segment in the BN-Lx and SHR parental strains. SHR.BN16 congenic rats had significantly lower weight, decreased concentrations of total triglycerides and cholesterol, and improved glucose tolerance compared with SHR rats. The concentrations of insulin, free fatty acids, and adiponectin were comparable between the two strains. SHR.BN16 rats had significantly lower systolic (18-28 mmHg difference) and diastolic (10-15 mmHg difference) blood pressure throughout the experiment (repeated-measures ANOVA, P < 0.001). The differential segment spans approximately 22 Mb of the telomeric part of the short arm of RNO16. The in silico analyses revealed over 1200 DNA variants between the BN-Lx and SHR genomes in the SHR.BN16 differential segment, 44 of which lead to missense mutations, and only eight of which (in Asb14, Il17rd, Itih1, Syt15, Ercc6, RGD1564958, Tmem161a, and Gatad2a genes) are predicted to be damaging to the protein product. Furthermore, a number of genes within the RNO16 differential segment associated with metabolic syndrome components in human studies showed polymorphisms between SHR and BN-Lx (including Lpl, Nrg3, Pbx4, Cilp2, and Stab1). Our novel congenic rat model demonstrates that a limited genomic region on RNO16 in the SHR significantly affects many of the features of metabolic syndrome.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>27031336</pmid><doi>10.1371/journal.pone.0152708</doi><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2016-03, Vol.11 (3), p.e0152708-e0152708 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1777534041 |
| source | PubMed Central Free; MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS) Journals Open Access; EZB-FREE-00999 freely available EZB journals; Free Full-Text Journals in Chemistry |
| subjects | Adiponectin Animals Animals, Congenic - genetics Animals, Congenic - metabolism Animals, Congenic - physiology Biology Biology and Life Sciences Blood pressure Cholesterol Chromosome 16 Chromosomes Chromosomes, Human, Pair 16 - genetics Comparative analysis Deoxyribonucleic acid Diabetes DNA Fatty acids Gene expression Gene sequencing Genes Genetic aspects Genetic polymorphisms Genetics Genome Genomes Genomics Glucose tolerance Glucose Tolerance Test Hemodynamics Humans Hypertension Insulin Insulin resistance Interleukin 1 Male Medicine Medicine and Health Sciences Metabolic syndrome Metabolic Syndrome - genetics Metabolic Syndrome - metabolism Metabolic Syndrome - physiopathology Metabolic syndrome X Metabolome Missense mutation Mutation Nucleotide sequence Physiological aspects Physiology Rats Rats, Inbred BN - genetics Rats, Inbred BN - metabolism Rats, Inbred BN - physiology Rats, Inbred SHR - genetics Rats, Inbred SHR - metabolism Rats, Inbred SHR - physiology Research and Analysis Methods Risk factors Rodents Studies Synteny Triglycerides Variance analysis |
| title | Isolation of a Genomic Region Affecting Most Components of Metabolic Syndrome in a Chromosome-16 Congenic Rat Model |
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