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Interrelationships Between the Kinetics of VLDL Subspecies and HDL Catabolism in Abdominal Obesity: A Multicenter Tracer Kinetic Study

Identifieur interne : 004089 ( Main/Exploration ); précédent : 004088; suivant : 004090

Interrelationships Between the Kinetics of VLDL Subspecies and HDL Catabolism in Abdominal Obesity: A Multicenter Tracer Kinetic Study

Auteurs : Bruno Verges [France] ; Martin Adiels [Suède] ; Jan Boren [Suède] ; Peter Hugh Barrett [Australie] ; Gerald F. Watts [Australie] ; Dick Chan [Australie] ; Laurence Duvillard [France] ; Sanni Söderlund [Finlande] ; Niina Matikainen [Finlande] ; Juhani Kahri [Finlande] ; Isabelle Robin [France] ; Marja-Riitta Taskinen [Finlande]

Source :

RBID : Pascal:15-0000333

Descripteurs français

English descriptors

Abstract

Context: Low plasma high-density lipoprotein (HDL) cholesterol is a major abnormality in abdominal obesity. This relates due to accelerated HDL catabolism, but the underlying mechanism requires further elucidation. The relationships between HDL catabolism and other variables that may be modified in abdominal obesity, such as very low-density lipoprotein (VLDL) subspecies (VLDL, VLDL2) kinetics, liver fat, or visceral adiposity, remain to be investigated. Objectives: Our aim was to study the associations between HDL apolipoprotein (apo)-A-l fractional catabolic rate (FCR) and the kinetics of VLDL subspecies and estimates of liver and visceral and sc fat. Design: We carried out a multicenter in vivo kinetic study using stable isotopes (deuterated leucine and glycerol) in 62 individuals with abdominal obesity. Results: In a multivariate analysis, among the morphological and biological parameters that may predict apoA-1 FCR, liver fat (β = .400, P = .003), and VLDL1-apoB (β = .307, P = .020) were independently associated with apoA-I FCR. In a multivariate analysis, among the kinetic parameters, VLDL1-triglycerides (TGs) indirect FCR (β = -.357, P = .001), VLDL,-TG production rate (β = 0.213, P = .048), and apoA-II FCR (β = .667, P < .0001) were independently associated with apoA-I FCR. After adjustment for VLDL1-TG production rate, liver fat was no more correlated with apoA-I FCR. No association between apoA-I FCR and visceral fat was observed. Conclusions: We show that VLDL, is an important independent determinant of apoA-I FCR and more precisely that apoA-I FCR is independently associated with both catabolism and the production of VLDL1-TG. In addition, we show an association between liver fat and apoA-I FCR that is mostly mediated by VLDL1-TG production. These data indicate that, in abdominal obesity, dysfunctional VLDL1 metabolism is an important modulator of HDL apoA-I catabolism.


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Le document en format XML

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<name sortKey="Kahri, Juhani" sort="Kahri, Juhani" uniqKey="Kahri J" first="Juhani" last="Kahri">Juhani Kahri</name>
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</author>
<author>
<name sortKey="Taskinen, Marja Riitta" sort="Taskinen, Marja Riitta" uniqKey="Taskinen M" first="Marja-Riitta" last="Taskinen">Marja-Riitta Taskinen</name>
<affiliation wicri:level="1">
<inist:fA14 i1="08">
<s1>Heart and Lung Centre, Helsinki University Central Hospital and Research Programs' Unit, Department of Diabetes and Obesity, University of Helsinki, Helsinki University Central Hospital</s1>
<s2>00290 Helsinki</s2>
<s3>FIN</s3>
<sZ>8 aut.</sZ>
<sZ>9 aut.</sZ>
<sZ>12 aut.</sZ>
</inist:fA14>
<country>Finlande</country>
<wicri:noRegion>00290 Helsinki</wicri:noRegion>
</affiliation>
</author>
</analytic>
<series>
<title level="j" type="main">The Journal of clinical endocrinology and metabolism</title>
<title level="j" type="abbreviated">J. clin. endocrinol. metab.</title>
<idno type="ISSN">0021-972X</idno>
<imprint>
<date when="2014">2014</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
<seriesStmt>
<title level="j" type="main">The Journal of clinical endocrinology and metabolism</title>
<title level="j" type="abbreviated">J. clin. endocrinol. metab.</title>
<idno type="ISSN">0021-972X</idno>
</seriesStmt>
</fileDesc>
<profileDesc>
<textClass>
<keywords scheme="KwdEn" xml:lang="en">
<term>Catabolism</term>
<term>Endocrinology</term>
<term>Kinetics</term>
<term>Lipoprotein HDL</term>
<term>Lipoprotein VLDL</term>
<term>Metabolic diseases</term>
<term>Multicenter study</term>
<term>Nutrition</term>
<term>Tracers</term>
<term>Visceral obesity</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr">
<term>Obésité viscérale</term>
<term>Cinétique</term>
<term>Lipoprotéine VLDL</term>
<term>Lipoprotéine HDL</term>
<term>Catabolisme</term>
<term>Etude multicentrique</term>
<term>Traceur</term>
<term>Endocrinologie</term>
<term>Maladie métabolique</term>
<term>Nutrition</term>
</keywords>
<keywords scheme="Wicri" type="topic" xml:lang="fr">
<term>Nutrition</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front>
<div type="abstract" xml:lang="en">Context: Low plasma high-density lipoprotein (HDL) cholesterol is a major abnormality in abdominal obesity. This relates due to accelerated HDL catabolism, but the underlying mechanism requires further elucidation. The relationships between HDL catabolism and other variables that may be modified in abdominal obesity, such as very low-density lipoprotein (VLDL) subspecies (VLDL, VLDL
<sub>2</sub>
) kinetics, liver fat, or visceral adiposity, remain to be investigated. Objectives: Our aim was to study the associations between HDL apolipoprotein (apo)-A-l fractional catabolic rate (FCR) and the kinetics of VLDL subspecies and estimates of liver and visceral and sc fat. Design: We carried out a multicenter in vivo kinetic study using stable isotopes (deuterated leucine and glycerol) in 62 individuals with abdominal obesity. Results: In a multivariate analysis, among the morphological and biological parameters that may predict apoA-1 FCR, liver fat (β = .400, P = .003), and VLDL
<sub>1</sub>
-apoB (β = .307, P = .020) were independently associated with apoA-I FCR. In a multivariate analysis, among the kinetic parameters, VLDL
<sub>1</sub>
-triglycerides (TGs) indirect FCR (β = -.357, P = .001), VLDL,-TG production rate (β = 0.213, P = .048), and apoA-II FCR (β = .667, P < .0001) were independently associated with apoA-I FCR. After adjustment for VLDL1-TG production rate, liver fat was no more correlated with apoA-I FCR. No association between apoA-I FCR and visceral fat was observed. Conclusions: We show that VLDL, is an important independent determinant of apoA-I FCR and more precisely that apoA-I FCR is independently associated with both catabolism and the production of VLDL
<sub>1</sub>
-TG. In addition, we show an association between liver fat and apoA-I FCR that is mostly mediated by VLDL
<sub>1</sub>
-TG production. These data indicate that, in abdominal obesity, dysfunctional VLDL
<sub>1</sub>
metabolism is an important modulator of HDL apoA-I catabolism.</div>
</front>
</TEI>
<affiliations>
<list>
<country>
<li>Australie</li>
<li>Finlande</li>
<li>France</li>
<li>Suède</li>
</country>
<region>
<li>Bourgogne</li>
<li>Bourgogne-Franche-Comté</li>
</region>
<settlement>
<li>Dijon</li>
</settlement>
</list>
<tree>
<country name="France">
<region name="Bourgogne-Franche-Comté">
<name sortKey="Verges, Bruno" sort="Verges, Bruno" uniqKey="Verges B" first="Bruno" last="Verges">Bruno Verges</name>
</region>
<name sortKey="Duvillard, Laurence" sort="Duvillard, Laurence" uniqKey="Duvillard L" first="Laurence" last="Duvillard">Laurence Duvillard</name>
<name sortKey="Duvillard, Laurence" sort="Duvillard, Laurence" uniqKey="Duvillard L" first="Laurence" last="Duvillard">Laurence Duvillard</name>
<name sortKey="Robin, Isabelle" sort="Robin, Isabelle" uniqKey="Robin I" first="Isabelle" last="Robin">Isabelle Robin</name>
<name sortKey="Verges, Bruno" sort="Verges, Bruno" uniqKey="Verges B" first="Bruno" last="Verges">Bruno Verges</name>
</country>
<country name="Suède">
<noRegion>
<name sortKey="Adiels, Martin" sort="Adiels, Martin" uniqKey="Adiels M" first="Martin" last="Adiels">Martin Adiels</name>
</noRegion>
<name sortKey="Adiels, Martin" sort="Adiels, Martin" uniqKey="Adiels M" first="Martin" last="Adiels">Martin Adiels</name>
<name sortKey="Boren, Jan" sort="Boren, Jan" uniqKey="Boren J" first="Jan" last="Boren">Jan Boren</name>
</country>
<country name="Australie">
<noRegion>
<name sortKey="Barrett, Peter Hugh" sort="Barrett, Peter Hugh" uniqKey="Barrett P" first="Peter Hugh" last="Barrett">Peter Hugh Barrett</name>
</noRegion>
<name sortKey="Barrett, Peter Hugh" sort="Barrett, Peter Hugh" uniqKey="Barrett P" first="Peter Hugh" last="Barrett">Peter Hugh Barrett</name>
<name sortKey="Chan, Dick" sort="Chan, Dick" uniqKey="Chan D" first="Dick" last="Chan">Dick Chan</name>
<name sortKey="Watts, Gerald F" sort="Watts, Gerald F" uniqKey="Watts G" first="Gerald F." last="Watts">Gerald F. Watts</name>
</country>
<country name="Finlande">
<noRegion>
<name sortKey="Soderlund, Sanni" sort="Soderlund, Sanni" uniqKey="Soderlund S" first="Sanni" last="Söderlund">Sanni Söderlund</name>
</noRegion>
<name sortKey="Kahri, Juhani" sort="Kahri, Juhani" uniqKey="Kahri J" first="Juhani" last="Kahri">Juhani Kahri</name>
<name sortKey="Matikainen, Niina" sort="Matikainen, Niina" uniqKey="Matikainen N" first="Niina" last="Matikainen">Niina Matikainen</name>
<name sortKey="Matikainen, Niina" sort="Matikainen, Niina" uniqKey="Matikainen N" first="Niina" last="Matikainen">Niina Matikainen</name>
<name sortKey="Taskinen, Marja Riitta" sort="Taskinen, Marja Riitta" uniqKey="Taskinen M" first="Marja-Riitta" last="Taskinen">Marja-Riitta Taskinen</name>
</country>
</tree>
</affiliations>
</record>

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