Statin action favors normalization of the plasma lipidome in the atherogenic mixed dyslipidemia of MetS: potential relevance to statin-associated dysglycemia[S]
Identifieur interne : 002539 ( Pmc/Curation ); précédent : 002538; suivant : 002540Statin action favors normalization of the plasma lipidome in the atherogenic mixed dyslipidemia of MetS: potential relevance to statin-associated dysglycemia[S]
Auteurs : Peter J. Meikle ; Gerard Wong ; Ricardo Tan ; Philippe Giral ; Paul Robillard ; Alexina Orsoni ; Neil Hounslow ; Dianna J. Magliano ; Jonathan E. Shaw ; Joanne E. Curran ; John Blangero ; Bronwyn A. Kingwell ; M. John ChapmanSource :
- Journal of Lipid Research [ 0022-2275 ] ; 2015.
Abstract
The impact of statin treatment on the abnormal plasma lipidome of mixed dyslipidemic patients with metabolic syndrome (MetS), a group at increased risk of developing diabetes, was evaluated. Insulin-resistant hypertriglyceridemic hypertensive obese males (n = 12) displaying MetS were treated with pitavastatin (4 mg/day) for 180 days; healthy normolipidemic age-matched nonobese males (n = 12) acted as controls. Statin treatment substantially normalized triglyceride (−41%), remnant cholesterol (−55%), and LDL-cholesterol (−39%), with minor effect on HDL-cholesterol (+4%). Lipidomic analysis, normalized to nonHDL-cholesterol in order to probe statin-induced differences in molecular composition independently of reduction in plasma cholesterol, revealed increment in 132 of 138 lipid species that were subnormal at baseline and significantly shifted toward the control group on statin treatment. Increment in alkyl- and alkenylphospholipids (plasmalogens) was prominent, and consistent with significant statin-induced increase in plasma polyunsaturated fatty acid levels. Comparison of the statin-mediated lipidomic changes in MetS with the abnormal plasma lipidomic profile characteristic of prediabetes and T2D in the Australian Diabetes, Obesity, and Lifestyle Study and San Antonio Family Heart Study cohorts by hypergeometric analysis revealed a significant shift toward the lipid profile of controls, indicative of a marked trend toward a normolipidemic phenotype. Pitavastatin attenuated the abnormal plasma lipidome of MetS patients typical of prediabetes and T2D.
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DOI: 10.1194/jlr.P061143
PubMed: 26486974
PubMed Central: 4655992
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Magliano</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Shaw, Jonathan E" sort="Shaw, Jonathan E" uniqKey="Shaw J" first="Jonathan E." last="Shaw">Jonathan E. Shaw</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Curran, Joanne E" sort="Curran, Joanne E" uniqKey="Curran J" first="Joanne E." last="Curran">Joanne E. Curran</name><affiliation><nlm:aff id="aff4"></nlm:aff></affiliation></author><author><name sortKey="Blangero, John" sort="Blangero, John" uniqKey="Blangero J" first="John" last="Blangero">John Blangero</name><affiliation><nlm:aff id="aff4"></nlm:aff></affiliation></author><author><name sortKey="Kingwell, Bronwyn A" sort="Kingwell, Bronwyn A" uniqKey="Kingwell B" first="Bronwyn A." last="Kingwell">Bronwyn A. Kingwell</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Chapman, M John" sort="Chapman, M John" uniqKey="Chapman M" first="M. John" last="Chapman">M. John Chapman</name><affiliation><nlm:aff id="aff2"></nlm:aff></affiliation></author></analytic><series><title level="j">Journal of Lipid Research</title><idno type="ISSN">0022-2275</idno><idno type="eISSN">1539-7262</idno><imprint><date when="2015">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>The impact of statin treatment on the abnormal plasma lipidome of mixed dyslipidemic patients with metabolic syndrome (MetS), a group at increased risk of developing diabetes, was evaluated. Insulin-resistant hypertriglyceridemic hypertensive obese males (n = 12) displaying MetS were treated with pitavastatin (4 mg/day) for 180 days; healthy normolipidemic age-matched nonobese males (n = 12) acted as controls. Statin treatment substantially normalized triglyceride (−41%), remnant cholesterol (−55%), and LDL-cholesterol (−39%), with minor effect on HDL-cholesterol (+4%). Lipidomic analysis, normalized to nonHDL-cholesterol in order to probe statin-induced differences in molecular composition independently of reduction in plasma cholesterol, revealed increment in 132 of 138 lipid species that were subnormal at baseline and significantly shifted toward the control group on statin treatment. Increment in alkyl- and alkenylphospholipids (plasmalogens) was prominent, and consistent with significant statin-induced increase in plasma polyunsaturated fatty acid levels. Comparison of the statin-mediated lipidomic changes in MetS with the abnormal plasma lipidomic profile characteristic of prediabetes and T2D in the Australian Diabetes, Obesity, and Lifestyle Study and San Antonio Family Heart Study cohorts by hypergeometric analysis revealed a significant shift toward the lipid profile of controls, indicative of a marked trend toward a normolipidemic phenotype. Pitavastatin attenuated the abnormal plasma lipidome of MetS patients typical of prediabetes and T2D.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Baigent, C" uniqKey="Baigent C">C. Baigent</name></author><author><name sortKey="Blackwell, L" uniqKey="Blackwell L">L. Blackwell</name></author><author><name sortKey="Emberson, J" uniqKey="Emberson J">J. Emberson</name></author><author><name sortKey="Holland, L E" uniqKey="Holland L">L. E. Holland</name></author><author><name sortKey="Reith, C" uniqKey="Reith C">C. 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<front><journal-meta><journal-id journal-id-type="nlm-ta">J Lipid Res</journal-id><journal-id journal-id-type="iso-abbrev">J. Lipid Res</journal-id><journal-id journal-id-type="hwp">jlr</journal-id><journal-id journal-id-type="pmc">jlr</journal-id><journal-id journal-id-type="publisher-id">jlr</journal-id><journal-title-group><journal-title>Journal of Lipid Research</journal-title></journal-title-group><issn pub-type="ppub">0022-2275</issn><issn pub-type="epub">1539-7262</issn><publisher><publisher-name>The American Society for Biochemistry and Molecular Biology</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">26486974</article-id><article-id pub-id-type="pmc">4655992</article-id><article-id pub-id-type="publisher-id">p061143</article-id><article-id pub-id-type="doi">10.1194/jlr.P061143</article-id><article-categories><subj-group subj-group-type="heading"><subject>Patient-Oriented and Epidemiological Research</subject></subj-group></article-categories><title-group><article-title>Statin action favors normalization of the plasma lipidome in the atherogenic mixed dyslipidemia of MetS: potential relevance to statin-associated dysglycemia<xref ref-type="fn" rid="fn1">[S]</xref></article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Meikle</surname><given-names>Peter J.</given-names></name><xref ref-type="corresp" rid="cor1"><sup>1</sup></xref><xref ref-type="aff" rid="aff1">*</xref></contrib><contrib contrib-type="author"><name><surname>Wong</surname><given-names>Gerard</given-names></name><xref ref-type="aff" rid="aff1">*</xref></contrib><contrib contrib-type="author"><name><surname>Tan</surname><given-names>Ricardo</given-names></name><xref ref-type="aff" rid="aff1">*</xref></contrib><contrib contrib-type="author"><name><surname>Giral</surname><given-names>Philippe</given-names></name><xref ref-type="aff" rid="aff2">†</xref></contrib><contrib contrib-type="author"><name><surname>Robillard</surname><given-names>Paul</given-names></name><xref ref-type="aff" rid="aff2">†</xref></contrib><contrib contrib-type="author"><name><surname>Orsoni</surname><given-names>Alexina</given-names></name><xref ref-type="aff" rid="aff2">†</xref></contrib><contrib contrib-type="author"><name><surname>Hounslow</surname><given-names>Neil</given-names></name><xref ref-type="aff" rid="aff3">§</xref></contrib><contrib contrib-type="author"><name><surname>Magliano</surname><given-names>Dianna J.</given-names></name><xref ref-type="aff" rid="aff1">*</xref></contrib><contrib contrib-type="author"><name><surname>Shaw</surname><given-names>Jonathan E.</given-names></name><xref ref-type="aff" rid="aff1">*</xref></contrib><contrib contrib-type="author"><name><surname>Curran</surname><given-names>Joanne E.</given-names></name><xref ref-type="aff" rid="aff4">**</xref></contrib><contrib contrib-type="author"><name><surname>Blangero</surname><given-names>John</given-names></name><xref ref-type="aff" rid="aff4">**</xref></contrib><contrib contrib-type="author"><name><surname>Kingwell</surname><given-names>Bronwyn A.</given-names></name><xref ref-type="aff" rid="aff1">*</xref></contrib><contrib contrib-type="author"><name><surname>Chapman</surname><given-names>M. John</given-names></name><xref ref-type="aff" rid="aff2">†</xref></contrib><aff id="aff1"><institution>Baker IDI Heart and Diabetes Institute</institution>,<label>*</label> Melbourne,<country>Australia</country></aff><aff id="aff2">Dyslipidemia and Atherosclerosis Research Unit,<label>†</label> INSERM UMR-S939, and University of Pierre and Marie Curie,<institution>Pitie-Salpetriere University Hospital</institution>, Paris,<country>France</country></aff><aff id="aff3"><institution>Kowa Research Europe Ltd.</institution>,<label>§</label> Wokingham,<country>United Kingdom</country></aff><aff id="aff4">South Texas Diabetes and Obesity Institute,<label>**</label><institution>University of Texas Health Science Center at San Antonio</institution>, Harlingen,<addr-line>TX</addr-line></aff></contrib-group><author-notes><corresp id="cor1"><label>1</label>To whom correspondence should be addressed. e-mail: <email>peter.meikle@bakeridi.edu.au</email></corresp></author-notes><pub-date pub-type="epub-ppub"><month>12</month><year>2015</year></pub-date><pmc-comment>Fake ppub date generated by PMC from publisher
pub-date/@pub-type='epub-ppub' </pmc-comment>
<pub-date pub-type="ppub"><month>12</month><year>2015</year></pub-date><volume>56</volume><issue>12</issue><fpage>2381</fpage><lpage>2392</lpage><history><date date-type="received"><day>3</day><month>6</month><year>2015</year></date><date date-type="rev-recd"><day>17</day><month>10</month><year>2015</year></date></history><permissions><copyright-statement>Copyright © 2015 by the American Society for Biochemistry and Molecular Biology, Inc.</copyright-statement><copyright-year>2015</copyright-year><license license-type="open-access" xlink:href="http://creativecommons.org/licenses/by/4.0/"><license-p><italic><bold>Author’s Choice</bold>—Final version free via Creative Commons CC-BY license.</italic></license-p></license></permissions><abstract><p>The impact of statin treatment on the abnormal plasma lipidome of mixed dyslipidemic patients with metabolic syndrome (MetS), a group at increased risk of developing diabetes, was evaluated. Insulin-resistant hypertriglyceridemic hypertensive obese males (n = 12) displaying MetS were treated with pitavastatin (4 mg/day) for 180 days; healthy normolipidemic age-matched nonobese males (n = 12) acted as controls. Statin treatment substantially normalized triglyceride (−41%), remnant cholesterol (−55%), and LDL-cholesterol (−39%), with minor effect on HDL-cholesterol (+4%). Lipidomic analysis, normalized to nonHDL-cholesterol in order to probe statin-induced differences in molecular composition independently of reduction in plasma cholesterol, revealed increment in 132 of 138 lipid species that were subnormal at baseline and significantly shifted toward the control group on statin treatment. Increment in alkyl- and alkenylphospholipids (plasmalogens) was prominent, and consistent with significant statin-induced increase in plasma polyunsaturated fatty acid levels. Comparison of the statin-mediated lipidomic changes in MetS with the abnormal plasma lipidomic profile characteristic of prediabetes and T2D in the Australian Diabetes, Obesity, and Lifestyle Study and San Antonio Family Heart Study cohorts by hypergeometric analysis revealed a significant shift toward the lipid profile of controls, indicative of a marked trend toward a normolipidemic phenotype. Pitavastatin attenuated the abnormal plasma lipidome of MetS patients typical of prediabetes and T2D.</p></abstract><kwd-group><kwd>lipidomics</kwd><kwd>obesity</kwd><kwd>plasmalogens</kwd><kwd>cholesterol</kwd><kwd>omega-3 fatty acids</kwd><kwd>pitavastatin</kwd><kwd>metabolic syndrome</kwd></kwd-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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