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Postprandial lipemia and cardiovascular disease risk: Interrelationships between dietary, physiological and genetic determinants
Although the independence of the association and causality has not been fully established, non-fasting (postprandial) triglyceride (TG) concentrations have emerged as a clinically significant cardiovascular disease (CVD) risk factor. In the current review, findings from three insightful prospective...
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Published in: | Atherosclerosis 2012-01, Vol.220 (1), p.22-33 |
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description | Although the independence of the association and causality has not been fully established, non-fasting (postprandial) triglyceride (TG) concentrations have emerged as a clinically significant cardiovascular disease (CVD) risk factor. In the current review, findings from three insightful prospective studies in the area, namely the Women's Health Study, the Copenhagen City Heart Study and the Norwegian Counties Study, are discussed. An overview is provided as to the likely etiological basis for the association between postprandial TG and CVD, with a focus on both lipid and non-lipid (inflammation, hemostasis and vascular function) risk factors. The impact of various lifestyle and physiological determinants are considered, in particular genetic variation and meal fat composition. Furthermore, although data is limited some information is provided as to the relative and interactive impact of a number of modulators of lipemia. It is evident that relative to age, gender and body mass index (known modulators of postprandial lipemia), the contribution of identified gene variants to the heterogeneity observed in the postprandial response is likely to be relatively small. Finally, we highlight the need for the development of a standardised ‘fat tolerance test’ for use in clinical trials, to allow the integration and comparison of data from individual studies. |
doi_str_mv | 10.1016/j.atherosclerosis.2011.08.012 |
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In the current review, findings from three insightful prospective studies in the area, namely the Women's Health Study, the Copenhagen City Heart Study and the Norwegian Counties Study, are discussed. An overview is provided as to the likely etiological basis for the association between postprandial TG and CVD, with a focus on both lipid and non-lipid (inflammation, hemostasis and vascular function) risk factors. The impact of various lifestyle and physiological determinants are considered, in particular genetic variation and meal fat composition. Furthermore, although data is limited some information is provided as to the relative and interactive impact of a number of modulators of lipemia. It is evident that relative to age, gender and body mass index (known modulators of postprandial lipemia), the contribution of identified gene variants to the heterogeneity observed in the postprandial response is likely to be relatively small. Finally, we highlight the need for the development of a standardised ‘fat tolerance test’ for use in clinical trials, to allow the integration and comparison of data from individual studies.</description><identifier>ISSN: 0021-9150</identifier><identifier>EISSN: 1879-1484</identifier><identifier>DOI: 10.1016/j.atherosclerosis.2011.08.012</identifier><identifier>PMID: 21955695</identifier><language>eng</language><publisher>Amsterdam: Elsevier Ireland Ltd</publisher><subject>atherosclerosis ; Atherosclerosis (general aspects, experimental research) ; Biological and medical sciences ; Blood and lymphatic vessels ; Blood Vessels - physiopathology ; body mass index ; Cardiology. Vascular system ; Cardiovascular ; Cardiovascular Diseases - blood ; Cardiovascular Diseases - etiology ; Cardiovascular Diseases - genetics ; Cardiovascular Diseases - physiopathology ; clinical trials ; Coronary heart disease ; Diet - adverse effects ; Fat composition ; gender ; genes ; Genetic Predisposition to Disease ; genetic variation ; Genotype ; Heart ; Hemostasis ; Humans ; hyperlipidemia ; Hyperlipidemias - blood ; Hyperlipidemias - etiology ; Hyperlipidemias - genetics ; Hyperlipidemias - physiopathology ; Inflammation ; Inflammation - etiology ; lifestyle ; Medical sciences ; Non-fasting triglycerides ; Postprandial lipemia ; Postprandial Period ; prospective studies ; risk ; Risk Assessment ; Risk Factors ; triacylglycerols ; Triglycerides - blood ; Vascular function ; women's health</subject><ispartof>Atherosclerosis, 2012-01, Vol.220 (1), p.22-33</ispartof><rights>Elsevier Ireland Ltd</rights><rights>2011 Elsevier Ireland Ltd</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c497t-776c9d7a917991c4426118116f7db0a7ef6a756743b434c93083fd7bda78f783</citedby><cites>FETCH-LOGICAL-c497t-776c9d7a917991c4426118116f7db0a7ef6a756743b434c93083fd7bda78f783</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=25399749$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21955695$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jackson, Kim G</creatorcontrib><creatorcontrib>Poppitt, Sally D</creatorcontrib><creatorcontrib>Minihane, Anne M</creatorcontrib><title>Postprandial lipemia and cardiovascular disease risk: Interrelationships between dietary, physiological and genetic determinants</title><title>Atherosclerosis</title><addtitle>Atherosclerosis</addtitle><description>Although the independence of the association and causality has not been fully established, non-fasting (postprandial) triglyceride (TG) concentrations have emerged as a clinically significant cardiovascular disease (CVD) risk factor. In the current review, findings from three insightful prospective studies in the area, namely the Women's Health Study, the Copenhagen City Heart Study and the Norwegian Counties Study, are discussed. An overview is provided as to the likely etiological basis for the association between postprandial TG and CVD, with a focus on both lipid and non-lipid (inflammation, hemostasis and vascular function) risk factors. The impact of various lifestyle and physiological determinants are considered, in particular genetic variation and meal fat composition. Furthermore, although data is limited some information is provided as to the relative and interactive impact of a number of modulators of lipemia. It is evident that relative to age, gender and body mass index (known modulators of postprandial lipemia), the contribution of identified gene variants to the heterogeneity observed in the postprandial response is likely to be relatively small. Finally, we highlight the need for the development of a standardised ‘fat tolerance test’ for use in clinical trials, to allow the integration and comparison of data from individual studies.</description><subject>atherosclerosis</subject><subject>Atherosclerosis (general aspects, experimental research)</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Blood Vessels - physiopathology</subject><subject>body mass index</subject><subject>Cardiology. Vascular system</subject><subject>Cardiovascular</subject><subject>Cardiovascular Diseases - blood</subject><subject>Cardiovascular Diseases - etiology</subject><subject>Cardiovascular Diseases - genetics</subject><subject>Cardiovascular Diseases - physiopathology</subject><subject>clinical trials</subject><subject>Coronary heart disease</subject><subject>Diet - adverse effects</subject><subject>Fat composition</subject><subject>gender</subject><subject>genes</subject><subject>Genetic Predisposition to Disease</subject><subject>genetic variation</subject><subject>Genotype</subject><subject>Heart</subject><subject>Hemostasis</subject><subject>Humans</subject><subject>hyperlipidemia</subject><subject>Hyperlipidemias - blood</subject><subject>Hyperlipidemias - etiology</subject><subject>Hyperlipidemias - genetics</subject><subject>Hyperlipidemias - physiopathology</subject><subject>Inflammation</subject><subject>Inflammation - etiology</subject><subject>lifestyle</subject><subject>Medical sciences</subject><subject>Non-fasting triglycerides</subject><subject>Postprandial lipemia</subject><subject>Postprandial Period</subject><subject>prospective studies</subject><subject>risk</subject><subject>Risk Assessment</subject><subject>Risk Factors</subject><subject>triacylglycerols</subject><subject>Triglycerides - blood</subject><subject>Vascular function</subject><subject>women's health</subject><issn>0021-9150</issn><issn>1879-1484</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><recordid>eNqNkkFvEzEQhVcIREPhL8BeKi4keHa9axsJJFS1pVIlkFrOlmPPJk4de7Gdotz46XiV0ENPXGxZ-ubN-L2pqjMgCyDQf9wsVF5jDEm76bRp0RCABeELAs2zagaciTlQTp9XM0IamAvoyEn1KqUNIYQy4C-rkwZE1_Wim1V_foSUx6i8scrVzo64taouz1qraGx4UEnvnIq1sQlVwjradP-pvvYZY0Snsg0-re2Y6iXm34i-gJhV3H-ox_U-2eDCyuoiPUmu0GO2ujZYqrfWK5_T6-rFoFzCN8f7tLq7vLg7_za_-X51ff71Zq6pYHnOWK-FYUoAEwI0pU0PwAH6gZklUQyHXrGuZ7Rd0pZq0RLeDoYtjWJ8YLw9rd4fZMcYfu0wZbm1SaNzymPYJSmg4aRvBRTy84HUxd4UcZBjtNvyIwlEThHIjXwSgZwikITLEkGpf3vstFtu0TxW__O8AGdHoHir3FDM10XjketaIRgVhXt34AYVpFoV4-XP29Kpm3LklLaFuDoQWIx7sBhl0ha9RmMj6ixNsP899JcnStpZPwV3j3tMm7CLvqQjQaZGEnk7bda0WACEcOih_Qscws-a</recordid><startdate>20120101</startdate><enddate>20120101</enddate><creator>Jackson, Kim G</creator><creator>Poppitt, Sally D</creator><creator>Minihane, Anne M</creator><general>Elsevier Ireland Ltd</general><general>Elsevier</general><scope>FBQ</scope><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>20120101</creationdate><title>Postprandial lipemia and cardiovascular disease risk: Interrelationships between dietary, physiological and genetic determinants</title><author>Jackson, Kim G ; Poppitt, Sally D ; Minihane, Anne M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c497t-776c9d7a917991c4426118116f7db0a7ef6a756743b434c93083fd7bda78f783</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>atherosclerosis</topic><topic>Atherosclerosis (general aspects, experimental research)</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Blood Vessels - physiopathology</topic><topic>body mass index</topic><topic>Cardiology. Vascular system</topic><topic>Cardiovascular</topic><topic>Cardiovascular Diseases - blood</topic><topic>Cardiovascular Diseases - etiology</topic><topic>Cardiovascular Diseases - genetics</topic><topic>Cardiovascular Diseases - physiopathology</topic><topic>clinical trials</topic><topic>Coronary heart disease</topic><topic>Diet - adverse effects</topic><topic>Fat composition</topic><topic>gender</topic><topic>genes</topic><topic>Genetic Predisposition to Disease</topic><topic>genetic variation</topic><topic>Genotype</topic><topic>Heart</topic><topic>Hemostasis</topic><topic>Humans</topic><topic>hyperlipidemia</topic><topic>Hyperlipidemias - blood</topic><topic>Hyperlipidemias - etiology</topic><topic>Hyperlipidemias - genetics</topic><topic>Hyperlipidemias - physiopathology</topic><topic>Inflammation</topic><topic>Inflammation - etiology</topic><topic>lifestyle</topic><topic>Medical sciences</topic><topic>Non-fasting triglycerides</topic><topic>Postprandial lipemia</topic><topic>Postprandial Period</topic><topic>prospective studies</topic><topic>risk</topic><topic>Risk Assessment</topic><topic>Risk Factors</topic><topic>triacylglycerols</topic><topic>Triglycerides - blood</topic><topic>Vascular function</topic><topic>women's health</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jackson, Kim G</creatorcontrib><creatorcontrib>Poppitt, Sally D</creatorcontrib><creatorcontrib>Minihane, Anne M</creatorcontrib><collection>AGRIS</collection><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>Atherosclerosis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jackson, Kim G</au><au>Poppitt, Sally D</au><au>Minihane, Anne M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Postprandial lipemia and cardiovascular disease risk: Interrelationships between dietary, physiological and genetic determinants</atitle><jtitle>Atherosclerosis</jtitle><addtitle>Atherosclerosis</addtitle><date>2012-01-01</date><risdate>2012</risdate><volume>220</volume><issue>1</issue><spage>22</spage><epage>33</epage><pages>22-33</pages><issn>0021-9150</issn><eissn>1879-1484</eissn><abstract>Although the independence of the association and causality has not been fully established, non-fasting (postprandial) triglyceride (TG) concentrations have emerged as a clinically significant cardiovascular disease (CVD) risk factor. In the current review, findings from three insightful prospective studies in the area, namely the Women's Health Study, the Copenhagen City Heart Study and the Norwegian Counties Study, are discussed. An overview is provided as to the likely etiological basis for the association between postprandial TG and CVD, with a focus on both lipid and non-lipid (inflammation, hemostasis and vascular function) risk factors. The impact of various lifestyle and physiological determinants are considered, in particular genetic variation and meal fat composition. Furthermore, although data is limited some information is provided as to the relative and interactive impact of a number of modulators of lipemia. It is evident that relative to age, gender and body mass index (known modulators of postprandial lipemia), the contribution of identified gene variants to the heterogeneity observed in the postprandial response is likely to be relatively small. Finally, we highlight the need for the development of a standardised ‘fat tolerance test’ for use in clinical trials, to allow the integration and comparison of data from individual studies.</abstract><cop>Amsterdam</cop><pub>Elsevier Ireland Ltd</pub><pmid>21955695</pmid><doi>10.1016/j.atherosclerosis.2011.08.012</doi><tpages>12</tpages></addata></record> |
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subjects | atherosclerosis Atherosclerosis (general aspects, experimental research) Biological and medical sciences Blood and lymphatic vessels Blood Vessels - physiopathology body mass index Cardiology. Vascular system Cardiovascular Cardiovascular Diseases - blood Cardiovascular Diseases - etiology Cardiovascular Diseases - genetics Cardiovascular Diseases - physiopathology clinical trials Coronary heart disease Diet - adverse effects Fat composition gender genes Genetic Predisposition to Disease genetic variation Genotype Heart Hemostasis Humans hyperlipidemia Hyperlipidemias - blood Hyperlipidemias - etiology Hyperlipidemias - genetics Hyperlipidemias - physiopathology Inflammation Inflammation - etiology lifestyle Medical sciences Non-fasting triglycerides Postprandial lipemia Postprandial Period prospective studies risk Risk Assessment Risk Factors triacylglycerols Triglycerides - blood Vascular function women's health |
title | Postprandial lipemia and cardiovascular disease risk: Interrelationships between dietary, physiological and genetic determinants |
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