Interrelationships between the kinetics of VLDL subspecies and hdl catabolism in abdominal obesity: A multicenter tracer kinetic study

B.L. Vergès, M. Adiels, J.B. Borén, Hugh Barrett, Gerald Watts, Dick Chan, L. Duvillard, S. Söderlund, N. Matikainen, J. Kahri, I. Robin, M.R. Taskinen

    Research output: Contribution to journalArticle

    10 Citations (Scopus)

    Abstract

    Copyright © 2014 by the Endocrine Society. Context: Low plasma high-density lipoprotein (HDL) cholesterol is a major abnormality in abdominal obesity. This relatesdueto acceleratedHDLcatabolism, but the underlyingmechanismrequires 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 (VLDL1, VLDL2) kinetics, liver fat, or visceral adiposity, remain to be investigated. Objectives: Our aim was to study the associations between HDL apolipoprotein (apo)-A-I fractional catabolic rate (FCR) and the kinetics of VLDL subspecies and estimates of liver and visceral and sc fat. Design: Wecarried 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-I 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), VLDL1-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: Weshow that VLDL1 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, weshowanassociationbetweenliver fatandapoA-IFCRthat ismostlymediated byVLDL1-TG production. These data indicate that, inabdominalobesity, dysfunctionalVLDL1metabolism is an important modulator of HDL apoA-I catabolism.
    Original languageEnglish
    Pages (from-to)4281-4290
    JournalJournal of Clinical Endocrinology and Metabolism
    Volume99
    Issue number11
    DOIs
    Publication statusPublished - 2014

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    Abdominal Obesity
    VLDL Lipoproteins
    Apolipoprotein A-I
    Kinetics
    Triglycerides
    Liver
    Fats
    Intra-Abdominal Fat
    HDL Lipoproteins
    Multivariate Analysis
    Apolipoprotein A-II
    Adiposity
    Apolipoproteins B
    Kinetic parameters
    Leucine
    Isotopes
    Glycerol
    HDL Cholesterol
    Modulators
    Plasmas

    Cite this

    Vergès, B.L. ; Adiels, M. ; Borén, J.B. ; Barrett, Hugh ; Watts, Gerald ; Chan, Dick ; Duvillard, L. ; Söderlund, S. ; Matikainen, N. ; Kahri, J. ; Robin, I. ; Taskinen, M.R. / Interrelationships between the kinetics of VLDL subspecies and hdl catabolism in abdominal obesity: A multicenter tracer kinetic study. In: Journal of Clinical Endocrinology and Metabolism. 2014 ; Vol. 99, No. 11. pp. 4281-4290.
    @article{040a9b48beb0459b8e02af550453f11a,
    title = "Interrelationships between the kinetics of VLDL subspecies and hdl catabolism in abdominal obesity: A multicenter tracer kinetic study",
    abstract = "Copyright {\circledC} 2014 by the Endocrine Society. Context: Low plasma high-density lipoprotein (HDL) cholesterol is a major abnormality in abdominal obesity. This relatesdueto acceleratedHDLcatabolism, but the underlyingmechanismrequires 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 (VLDL1, VLDL2) kinetics, liver fat, or visceral adiposity, remain to be investigated. Objectives: Our aim was to study the associations between HDL apolipoprotein (apo)-A-I fractional catabolic rate (FCR) and the kinetics of VLDL subspecies and estimates of liver and visceral and sc fat. Design: Wecarried 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-I 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), VLDL1-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: Weshow that VLDL1 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, weshowanassociationbetweenliver fatandapoA-IFCRthat ismostlymediated byVLDL1-TG production. These data indicate that, inabdominalobesity, dysfunctionalVLDL1metabolism is an important modulator of HDL apoA-I catabolism.",
    author = "B.L. Verg{\`e}s and M. Adiels and J.B. Bor{\'e}n and Hugh Barrett and Gerald Watts and Dick Chan and L. Duvillard and S. S{\"o}derlund and N. Matikainen and J. Kahri and I. Robin and M.R. Taskinen",
    year = "2014",
    doi = "10.1210/jc.2014-2365",
    language = "English",
    volume = "99",
    pages = "4281--4290",
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    publisher = "ENDOCRINE SOC",
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    }

    Interrelationships between the kinetics of VLDL subspecies and hdl catabolism in abdominal obesity: A multicenter tracer kinetic study. / Vergès, B.L.; Adiels, M.; Borén, J.B.; Barrett, Hugh; Watts, Gerald; Chan, Dick; Duvillard, L.; Söderlund, S.; Matikainen, N.; Kahri, J.; Robin, I.; Taskinen, M.R.

    In: Journal of Clinical Endocrinology and Metabolism, Vol. 99, No. 11, 2014, p. 4281-4290.

    Research output: Contribution to journalArticle

    TY - JOUR

    T1 - Interrelationships between the kinetics of VLDL subspecies and hdl catabolism in abdominal obesity: A multicenter tracer kinetic study

    AU - Vergès, B.L.

    AU - Adiels, M.

    AU - Borén, J.B.

    AU - Barrett, Hugh

    AU - Watts, Gerald

    AU - Chan, Dick

    AU - Duvillard, L.

    AU - Söderlund, S.

    AU - Matikainen, N.

    AU - Kahri, J.

    AU - Robin, I.

    AU - Taskinen, M.R.

    PY - 2014

    Y1 - 2014

    N2 - Copyright © 2014 by the Endocrine Society. Context: Low plasma high-density lipoprotein (HDL) cholesterol is a major abnormality in abdominal obesity. This relatesdueto acceleratedHDLcatabolism, but the underlyingmechanismrequires 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 (VLDL1, VLDL2) kinetics, liver fat, or visceral adiposity, remain to be investigated. Objectives: Our aim was to study the associations between HDL apolipoprotein (apo)-A-I fractional catabolic rate (FCR) and the kinetics of VLDL subspecies and estimates of liver and visceral and sc fat. Design: Wecarried 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-I 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), VLDL1-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: Weshow that VLDL1 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, weshowanassociationbetweenliver fatandapoA-IFCRthat ismostlymediated byVLDL1-TG production. These data indicate that, inabdominalobesity, dysfunctionalVLDL1metabolism is an important modulator of HDL apoA-I catabolism.

    AB - Copyright © 2014 by the Endocrine Society. Context: Low plasma high-density lipoprotein (HDL) cholesterol is a major abnormality in abdominal obesity. This relatesdueto acceleratedHDLcatabolism, but the underlyingmechanismrequires 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 (VLDL1, VLDL2) kinetics, liver fat, or visceral adiposity, remain to be investigated. Objectives: Our aim was to study the associations between HDL apolipoprotein (apo)-A-I fractional catabolic rate (FCR) and the kinetics of VLDL subspecies and estimates of liver and visceral and sc fat. Design: Wecarried 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-I 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), VLDL1-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: Weshow that VLDL1 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, weshowanassociationbetweenliver fatandapoA-IFCRthat ismostlymediated byVLDL1-TG production. These data indicate that, inabdominalobesity, dysfunctionalVLDL1metabolism is an important modulator of HDL apoA-I catabolism.

    U2 - 10.1210/jc.2014-2365

    DO - 10.1210/jc.2014-2365

    M3 - Article

    VL - 99

    SP - 4281

    EP - 4290

    JO - Journal of Endocrinology & Metabolism

    JF - Journal of Endocrinology & Metabolism

    SN - 0021-972X

    IS - 11

    ER -