Statin action favors normalization of the plasma lipidome in the atherogenic mixed dyslipidemia of MetS: potential relevance to statin-associated dysglycemia[S]
Identifieur interne : 002806 ( Main/Exploration ); précédent : 002805; suivant : 002807Statin 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.
Descripteurs français
- KwdFr :
- Adulte, Adulte d'âge moyen, Athérosclérose (sang), Athérosclérose (traitement médicamenteux), Cholestérol, Cholestérol HDL, Cholestérol LDL, Dyslipidémies (sang), Dyslipidémies (traitement médicamenteux), Femelle, Humains, Inhibiteurs de l'hydroxyméthylglutaryl-CoA réductase (usage thérapeutique), Lipoprotéines, Mâle, Sujet âgé, Syndrome métabolique X (sang), Syndrome métabolique X (traitement médicamenteux), Triglycéride, Troubles du métabolisme du glucose (), Troubles du métabolisme du glucose (sang).
- MESH :
- sang : Athérosclérose, Dyslipidémies, Syndrome métabolique X, Troubles du métabolisme du glucose.
- traitement médicamenteux : Athérosclérose, Dyslipidémies, Syndrome métabolique X.
- usage thérapeutique : Inhibiteurs de l'hydroxyméthylglutaryl-CoA réductase.
- Adulte, Adulte d'âge moyen, Cholestérol, Cholestérol HDL, Cholestérol LDL, Femelle, Humains, Lipoprotéines, Mâle, Sujet âgé, Triglycéride, Troubles du métabolisme du glucose.
English descriptors
- KwdEn :
- Adult, Aged, Atherosclerosis (blood), Atherosclerosis (drug therapy), Cholesterol, Cholesterol, HDL, Cholesterol, LDL, Dyslipidemias (blood), Dyslipidemias (drug therapy), Female, Glucose Metabolism Disorders (blood), Glucose Metabolism Disorders (chemically induced), Humans, Hydroxymethylglutaryl-CoA Reductase Inhibitors (therapeutic use), Lipoproteins, Male, Metabolic Syndrome X (blood), Metabolic Syndrome X (drug therapy), Middle Aged, Triglycerides.
- MESH :
- chemical , therapeutic use : Hydroxymethylglutaryl-CoA Reductase Inhibitors.
- chemical : Cholesterol, Cholesterol, HDL, Cholesterol, LDL, Lipoproteins, Triglycerides.
- blood : Atherosclerosis, Dyslipidemias, Glucose Metabolism Disorders, Metabolic Syndrome X.
- chemically induced : Glucose Metabolism Disorders.
- drug therapy : Atherosclerosis, Dyslipidemias, Metabolic Syndrome X.
- Adult, Aged, Female, Humans, Male, Middle Aged.
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.
Url:
DOI: 10.1194/jlr.P061143
PubMed: 26486974
PubMed Central: 4655992
Affiliations:
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Le document en format XML
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<series><title level="j">Journal of Lipid Research</title>
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<term>Aged</term>
<term>Atherosclerosis (blood)</term>
<term>Atherosclerosis (drug therapy)</term>
<term>Cholesterol</term>
<term>Cholesterol, HDL</term>
<term>Cholesterol, LDL</term>
<term>Dyslipidemias (blood)</term>
<term>Dyslipidemias (drug therapy)</term>
<term>Female</term>
<term>Glucose Metabolism Disorders (blood)</term>
<term>Glucose Metabolism Disorders (chemically induced)</term>
<term>Humans</term>
<term>Hydroxymethylglutaryl-CoA Reductase Inhibitors (therapeutic use)</term>
<term>Lipoproteins</term>
<term>Male</term>
<term>Metabolic Syndrome X (blood)</term>
<term>Metabolic Syndrome X (drug therapy)</term>
<term>Middle Aged</term>
<term>Triglycerides</term>
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<keywords scheme="KwdFr" xml:lang="fr"><term>Adulte</term>
<term>Adulte d'âge moyen</term>
<term>Athérosclérose (sang)</term>
<term>Athérosclérose (traitement médicamenteux)</term>
<term>Cholestérol</term>
<term>Cholestérol HDL</term>
<term>Cholestérol LDL</term>
<term>Dyslipidémies (sang)</term>
<term>Dyslipidémies (traitement médicamenteux)</term>
<term>Femelle</term>
<term>Humains</term>
<term>Inhibiteurs de l'hydroxyméthylglutaryl-CoA réductase (usage thérapeutique)</term>
<term>Lipoprotéines</term>
<term>Mâle</term>
<term>Sujet âgé</term>
<term>Syndrome métabolique X (sang)</term>
<term>Syndrome métabolique X (traitement médicamenteux)</term>
<term>Triglycéride</term>
<term>Troubles du métabolisme du glucose ()</term>
<term>Troubles du métabolisme du glucose (sang)</term>
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<keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Hydroxymethylglutaryl-CoA Reductase Inhibitors</term>
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<term>Cholesterol, HDL</term>
<term>Cholesterol, LDL</term>
<term>Lipoproteins</term>
<term>Triglycerides</term>
</keywords>
<keywords scheme="MESH" qualifier="blood" xml:lang="en"><term>Atherosclerosis</term>
<term>Dyslipidemias</term>
<term>Glucose Metabolism Disorders</term>
<term>Metabolic Syndrome X</term>
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<keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Glucose Metabolism Disorders</term>
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<term>Dyslipidemias</term>
<term>Metabolic Syndrome X</term>
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<term>Dyslipidémies</term>
<term>Syndrome métabolique X</term>
<term>Troubles du métabolisme du glucose</term>
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<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>
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<tree><noCountry><name sortKey="Blangero, John" sort="Blangero, John" uniqKey="Blangero J" first="John" last="Blangero">John Blangero</name>
<name sortKey="Chapman, M John" sort="Chapman, M John" uniqKey="Chapman M" first="M. John" last="Chapman">M. John Chapman</name>
<name sortKey="Curran, Joanne E" sort="Curran, Joanne E" uniqKey="Curran J" first="Joanne E." last="Curran">Joanne E. Curran</name>
<name sortKey="Giral, Philippe" sort="Giral, Philippe" uniqKey="Giral P" first="Philippe" last="Giral">Philippe Giral</name>
<name sortKey="Hounslow, Neil" sort="Hounslow, Neil" uniqKey="Hounslow N" first="Neil" last="Hounslow">Neil Hounslow</name>
<name sortKey="Kingwell, Bronwyn A" sort="Kingwell, Bronwyn A" uniqKey="Kingwell B" first="Bronwyn A." last="Kingwell">Bronwyn A. Kingwell</name>
<name sortKey="Magliano, Dianna J" sort="Magliano, Dianna J" uniqKey="Magliano D" first="Dianna J." last="Magliano">Dianna J. Magliano</name>
<name sortKey="Meikle, Peter J" sort="Meikle, Peter J" uniqKey="Meikle P" first="Peter J." last="Meikle">Peter J. Meikle</name>
<name sortKey="Orsoni, Alexina" sort="Orsoni, Alexina" uniqKey="Orsoni A" first="Alexina" last="Orsoni">Alexina Orsoni</name>
<name sortKey="Robillard, Paul" sort="Robillard, Paul" uniqKey="Robillard P" first="Paul" last="Robillard">Paul Robillard</name>
<name sortKey="Shaw, Jonathan E" sort="Shaw, Jonathan E" uniqKey="Shaw J" first="Jonathan E." last="Shaw">Jonathan E. Shaw</name>
<name sortKey="Tan, Ricardo" sort="Tan, Ricardo" uniqKey="Tan R" first="Ricardo" last="Tan">Ricardo Tan</name>
<name sortKey="Wong, Gerard" sort="Wong, Gerard" uniqKey="Wong G" first="Gerard" last="Wong">Gerard Wong</name>
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