Triglyceride-rich lipoprotein metabolism in women: roles of apoC-II and apoC-III

Esther M. Ooi, Dick C. Chan, L. Hodson, M. Adiels, J. Boren, F. Karpe, B.A. Fielding, Gerald F. Watts, Hugh H.R. Barrett

    Research output: Contribution to journalArticle

    5 Citations (Scopus)

    Abstract

    © 2016 Stichting European Society for Clinical Investigation Journal FoundationBackground: Experimental data suggest that apolipoprotein (apo) C-II and C-III regulate triglyceride-rich lipoprotein (TRL) metabolism, but there are limited studies in humans. We investigated the metabolic associations of TRLs with apoC-II and apoC-III concentrations and kinetics in women. Material and methods: The kinetics of plasma apoC-II, apoC-III and very low-density lipoprotein (VLDL) apoB-100 and triglycerides were measured in the postabsorptive state using stable isotopic techniques and compartmental modelling in 60 women with wide-ranging body mass index (19·5–32·9 kg/m2). Results: Plasma apoC-II and apoC-III concentrations were positively associated with the concentrations of plasma triglycerides, VLDL1- and VLDL2-apoB-100 and triglyceride (all P <0·05). ApoC-II production rate (PR) was positively associated with VLDL1-apoB-100 concentration, VLDL1 triglyceride concentration and VLDL1 triglyceride PR, while apoC-II fractional catabolic rate (FCR) was positively associated with VLDL1 triglyceride FCR (all P <0·05). No significant associations were observed between apoC-II and VLDL2 apoB-100 or triglyceride kinetics. ApoC-III PR, but not FCR, was positively associated with VLDL1 triglyceride, and VLDL2-apoB-100 and triglyceride concentrations (all P <0·05). No significant associations were observed between apoC-III and VLDL-apoB-100 and triglyceride kinetics. In multivariable analysis, including homoeostasis model assessment score, menopausal status and obesity, apoC-II concentration was significantly associated with plasma triglyceride, VLDL1-apoB-100 and VLDL1 triglyceride concentrations and PR. Using the same multivariable analysis, apoC-III was significantly associated with plasma triglyceride and VLDL1- and VLDL2-apoB-100 and triglyceride concentrations and FCR. Conclusions: In women, plasma apoC-II and apoC-III concentrations are regulated by their respective PR and are significant, independent determinants of the kin
    Original languageEnglish
    Pages (from-to)730-736
    Number of pages7
    JournalEuropean Journal of Clinical Investigation
    Volume46
    Issue number8
    DOIs
    Publication statusPublished - 2016

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    Apolipoprotein C-III
    Apolipoproteins C
    Metabolism
    Lipoproteins
    Triglycerides
    Apolipoprotein B-100
    Plasmas
    Kinetics
    VLDL Lipoproteins
    Apolipoprotein C-II

    Cite this

    @article{0a4d72ca596d4a08a95dabb5fa9b9d92,
    title = "Triglyceride-rich lipoprotein metabolism in women: roles of apoC-II and apoC-III",
    abstract = "{\circledC} 2016 Stichting European Society for Clinical Investigation Journal FoundationBackground: Experimental data suggest that apolipoprotein (apo) C-II and C-III regulate triglyceride-rich lipoprotein (TRL) metabolism, but there are limited studies in humans. We investigated the metabolic associations of TRLs with apoC-II and apoC-III concentrations and kinetics in women. Material and methods: The kinetics of plasma apoC-II, apoC-III and very low-density lipoprotein (VLDL) apoB-100 and triglycerides were measured in the postabsorptive state using stable isotopic techniques and compartmental modelling in 60 women with wide-ranging body mass index (19·5–32·9 kg/m2). Results: Plasma apoC-II and apoC-III concentrations were positively associated with the concentrations of plasma triglycerides, VLDL1- and VLDL2-apoB-100 and triglyceride (all P <0·05). ApoC-II production rate (PR) was positively associated with VLDL1-apoB-100 concentration, VLDL1 triglyceride concentration and VLDL1 triglyceride PR, while apoC-II fractional catabolic rate (FCR) was positively associated with VLDL1 triglyceride FCR (all P <0·05). No significant associations were observed between apoC-II and VLDL2 apoB-100 or triglyceride kinetics. ApoC-III PR, but not FCR, was positively associated with VLDL1 triglyceride, and VLDL2-apoB-100 and triglyceride concentrations (all P <0·05). No significant associations were observed between apoC-III and VLDL-apoB-100 and triglyceride kinetics. In multivariable analysis, including homoeostasis model assessment score, menopausal status and obesity, apoC-II concentration was significantly associated with plasma triglyceride, VLDL1-apoB-100 and VLDL1 triglyceride concentrations and PR. Using the same multivariable analysis, apoC-III was significantly associated with plasma triglyceride and VLDL1- and VLDL2-apoB-100 and triglyceride concentrations and FCR. Conclusions: In women, plasma apoC-II and apoC-III concentrations are regulated by their respective PR and are significant, independent determinants of the kin",
    author = "Ooi, {Esther M.} and Chan, {Dick C.} and L. Hodson and M. Adiels and J. Boren and F. Karpe and B.A. Fielding and Watts, {Gerald F.} and Barrett, {Hugh H.R.}",
    year = "2016",
    doi = "10.1111/eci.12657",
    language = "English",
    volume = "46",
    pages = "730--736",
    journal = "European Journal of Clinical Investigation",
    issn = "0014-2972",
    publisher = "Wiley-Blackwell",
    number = "8",

    }

    Triglyceride-rich lipoprotein metabolism in women: roles of apoC-II and apoC-III. / Ooi, Esther M.; Chan, Dick C.; Hodson, L.; Adiels, M.; Boren, J.; Karpe, F.; Fielding, B.A.; Watts, Gerald F.; Barrett, Hugh H.R.

    In: European Journal of Clinical Investigation, Vol. 46, No. 8, 2016, p. 730-736.

    Research output: Contribution to journalArticle

    TY - JOUR

    T1 - Triglyceride-rich lipoprotein metabolism in women: roles of apoC-II and apoC-III

    AU - Ooi, Esther M.

    AU - Chan, Dick C.

    AU - Hodson, L.

    AU - Adiels, M.

    AU - Boren, J.

    AU - Karpe, F.

    AU - Fielding, B.A.

    AU - Watts, Gerald F.

    AU - Barrett, Hugh H.R.

    PY - 2016

    Y1 - 2016

    N2 - © 2016 Stichting European Society for Clinical Investigation Journal FoundationBackground: Experimental data suggest that apolipoprotein (apo) C-II and C-III regulate triglyceride-rich lipoprotein (TRL) metabolism, but there are limited studies in humans. We investigated the metabolic associations of TRLs with apoC-II and apoC-III concentrations and kinetics in women. Material and methods: The kinetics of plasma apoC-II, apoC-III and very low-density lipoprotein (VLDL) apoB-100 and triglycerides were measured in the postabsorptive state using stable isotopic techniques and compartmental modelling in 60 women with wide-ranging body mass index (19·5–32·9 kg/m2). Results: Plasma apoC-II and apoC-III concentrations were positively associated with the concentrations of plasma triglycerides, VLDL1- and VLDL2-apoB-100 and triglyceride (all P <0·05). ApoC-II production rate (PR) was positively associated with VLDL1-apoB-100 concentration, VLDL1 triglyceride concentration and VLDL1 triglyceride PR, while apoC-II fractional catabolic rate (FCR) was positively associated with VLDL1 triglyceride FCR (all P <0·05). No significant associations were observed between apoC-II and VLDL2 apoB-100 or triglyceride kinetics. ApoC-III PR, but not FCR, was positively associated with VLDL1 triglyceride, and VLDL2-apoB-100 and triglyceride concentrations (all P <0·05). No significant associations were observed between apoC-III and VLDL-apoB-100 and triglyceride kinetics. In multivariable analysis, including homoeostasis model assessment score, menopausal status and obesity, apoC-II concentration was significantly associated with plasma triglyceride, VLDL1-apoB-100 and VLDL1 triglyceride concentrations and PR. Using the same multivariable analysis, apoC-III was significantly associated with plasma triglyceride and VLDL1- and VLDL2-apoB-100 and triglyceride concentrations and FCR. Conclusions: In women, plasma apoC-II and apoC-III concentrations are regulated by their respective PR and are significant, independent determinants of the kin

    AB - © 2016 Stichting European Society for Clinical Investigation Journal FoundationBackground: Experimental data suggest that apolipoprotein (apo) C-II and C-III regulate triglyceride-rich lipoprotein (TRL) metabolism, but there are limited studies in humans. We investigated the metabolic associations of TRLs with apoC-II and apoC-III concentrations and kinetics in women. Material and methods: The kinetics of plasma apoC-II, apoC-III and very low-density lipoprotein (VLDL) apoB-100 and triglycerides were measured in the postabsorptive state using stable isotopic techniques and compartmental modelling in 60 women with wide-ranging body mass index (19·5–32·9 kg/m2). Results: Plasma apoC-II and apoC-III concentrations were positively associated with the concentrations of plasma triglycerides, VLDL1- and VLDL2-apoB-100 and triglyceride (all P <0·05). ApoC-II production rate (PR) was positively associated with VLDL1-apoB-100 concentration, VLDL1 triglyceride concentration and VLDL1 triglyceride PR, while apoC-II fractional catabolic rate (FCR) was positively associated with VLDL1 triglyceride FCR (all P <0·05). No significant associations were observed between apoC-II and VLDL2 apoB-100 or triglyceride kinetics. ApoC-III PR, but not FCR, was positively associated with VLDL1 triglyceride, and VLDL2-apoB-100 and triglyceride concentrations (all P <0·05). No significant associations were observed between apoC-III and VLDL-apoB-100 and triglyceride kinetics. In multivariable analysis, including homoeostasis model assessment score, menopausal status and obesity, apoC-II concentration was significantly associated with plasma triglyceride, VLDL1-apoB-100 and VLDL1 triglyceride concentrations and PR. Using the same multivariable analysis, apoC-III was significantly associated with plasma triglyceride and VLDL1- and VLDL2-apoB-100 and triglyceride concentrations and FCR. Conclusions: In women, plasma apoC-II and apoC-III concentrations are regulated by their respective PR and are significant, independent determinants of the kin

    U2 - 10.1111/eci.12657

    DO - 10.1111/eci.12657

    M3 - Article

    VL - 46

    SP - 730

    EP - 736

    JO - European Journal of Clinical Investigation

    JF - European Journal of Clinical Investigation

    SN - 0014-2972

    IS - 8

    ER -