Is liver fat detrimental to vessels?: intersections in the pathogenesis of NAFLD and atherosclerosis.
Identifieur interne : 000133 ( PubMed/Corpus ); précédent : 000132; suivant : 000134Is liver fat detrimental to vessels?: intersections in the pathogenesis of NAFLD and atherosclerosis.
Auteurs : Paola Loria ; Amedeo Lonardo ; Giovanni TargherSource :
- Clinical science (London, England : 1979) [ 1470-8736 ] ; 2008.
English descriptors
- KwdEn :
- MESH :
- etiology : Atherosclerosis, Fatty Liver, Metabolic Syndrome X.
- physiopathology : Atherosclerosis, Endocrine System, Fatty Liver.
- Female, Humans, Lipid Metabolism, Male, Risk Factors.
Abstract
NAFLD (non-alcoholic fatty liver disease) encompasses the spectrum of fatty liver disease in insulin-resistant individuals who often display T2DM (Type 2 diabetes mellitus) and obesity. The present review highlights the pathophysiological basis and clinical evidence for a possible causal linkage between NAFLD and CVD (cardiovascular disease). The role of traditional and non-traditional CVD risk factors in the pathophysiology of NAFLD is considered in the first part of the review, with the basic science shared by atherogenesis and hepatic steatogenesis discussed in depth in the second part. In conclusion, NAFLD is not an innocent bystander, but a major player in the development and progression of CVD. NAFLD and CVD also share similar molecular mechanisms and targeted treatment strategies. On the research side, studies should focus on interventions aimed at restoring energy homoeostasis in lipotoxic tissues and at improving hepatic (micro)vascular blood supply.
DOI: 10.1042/CS20070311
PubMed: 19016656
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pubmed:19016656Le document en format XML
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The present review highlights the pathophysiological basis and clinical evidence for a possible causal linkage between NAFLD and CVD (cardiovascular disease). The role of traditional and non-traditional CVD risk factors in the pathophysiology of NAFLD is considered in the first part of the review, with the basic science shared by atherogenesis and hepatic steatogenesis discussed in depth in the second part. In conclusion, NAFLD is not an innocent bystander, but a major player in the development and progression of CVD. NAFLD and CVD also share similar molecular mechanisms and targeted treatment strategies. On the research side, studies should focus on interventions aimed at restoring energy homoeostasis in lipotoxic tissues and at improving hepatic (micro)vascular blood supply.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">19016656</PMID><DateCreated><Year>2008</Year><Month>11</Month><Day>21</Day></DateCreated><DateCompleted><Year>2009</Year><Month>01</Month><Day>07</Day></DateCompleted><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1470-8736</ISSN><JournalIssue CitedMedium="Internet"><Volume>115</Volume><Issue>1</Issue><PubDate><Year>2008</Year><Month>Jul</Month></PubDate></JournalIssue><Title>Clinical science (London, England : 1979)</Title><ISOAbbreviation>Clin. Sci.</ISOAbbreviation></Journal><ArticleTitle>Is liver fat detrimental to vessels?: intersections in the pathogenesis of NAFLD and atherosclerosis.</ArticleTitle><Pagination><MedlinePgn>1-12</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1042/CS20070311</ELocationID><Abstract><AbstractText>NAFLD (non-alcoholic fatty liver disease) encompasses the spectrum of fatty liver disease in insulin-resistant individuals who often display T2DM (Type 2 diabetes mellitus) and obesity. The present review highlights the pathophysiological basis and clinical evidence for a possible causal linkage between NAFLD and CVD (cardiovascular disease). The role of traditional and non-traditional CVD risk factors in the pathophysiology of NAFLD is considered in the first part of the review, with the basic science shared by atherogenesis and hepatic steatogenesis discussed in depth in the second part. In conclusion, NAFLD is not an innocent bystander, but a major player in the development and progression of CVD. NAFLD and CVD also share similar molecular mechanisms and targeted treatment strategies. On the research side, studies should focus on interventions aimed at restoring energy homoeostasis in lipotoxic tissues and at improving hepatic (micro)vascular blood supply.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Loria</LastName><ForeName>Paola</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Department of Internal Medicine, Metabolism, Endocrinology and Geriatrics, University of Modena and Reggio Emilia, Modena, Italy. loria.paola@unimore.it</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lonardo</LastName><ForeName>Amedeo</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Targher</LastName><ForeName>Giovanni</ForeName><Initials>G</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Clin Sci (Lond)</MedlineTA><NlmUniqueID>7905731</NlmUniqueID><ISSNLinking>0143-5221</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D050197">Atherosclerosis</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000209">etiology</QualifierName><QualifierName MajorTopicYN="N" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D004703">Endocrine System</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005234">Fatty Liver</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000209">etiology</QualifierName><QualifierName MajorTopicYN="N" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005260">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D050356">Lipid Metabolism</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008297">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D024821">Metabolic Syndrome X</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000209">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D012307">Risk Factors</DescriptorName></MeshHeading></MeshHeadingList><NumberOfReferences>155</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2008</Year><Month>11</Month><Day>20</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2009</Year><Month>1</Month><Day>8</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2008</Year><Month>11</Month><Day>20</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pii">CS20070311</ArticleId><ArticleId IdType="doi">10.1042/CS20070311</ArticleId><ArticleId IdType="pubmed">19016656</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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