The metabolic and pharmacologic bases for treating atherogenic dyslipidaemia

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    Abstract

    Dyslipoproteinaemia is a cardinal feature of the metabolic syndrome that accelerates atherosclerosis. It is characterized by high plasma concentrations of triglyceride-rich and apolipoprotein (apo) B-containing lipoproteins, with depressed high-density lipoprotein (HDL) and increased small dense low-density lipoprotein (LDL) particle concentrations. Dysregulation of lipoprotein metabolism in the metabolic syndrome may be due to a combination of overproduction of very-low density lipoprotein (VLDL) apoB, decreased catabolism of apoB-containing particles, and increased catabolism of HDL apoA-I particles. These abnormalities are due to a global metabolic effect of insulin resistance and visceral obesity. Lifestyle modifications (dietary restriction and increased exercise) and pharmacological treatments favourably alter lipoprotein transport by decreasing the hepatic secretion of VLDL-apoB and the catabolism of HDL apoA-I, as well as by increasing the clearance of LDL-apoB. The safety and tolerability of combination drug therapy based on statins is important and merits further investigation. There are several pipeline therapies for correcting triglyceride-rich lipoprotein and HDL metabolism. However, their clinical efficacy, safety and cost-effectiveness remain to be demonstrated. © 2014 Elsevier Inc. All rights reserved.
    Original languageEnglish
    Pages (from-to)369-385
    JournalBest Practice and Research: Clinical Endocrinology and Metabolism
    Volume28
    Issue number3
    DOIs
    Publication statusPublished - 2014

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    Apolipoproteins B
    Dyslipidemias
    HDL Lipoproteins
    Lipoproteins
    VLDL Lipoproteins
    Apolipoprotein A-I
    LDL Lipoproteins
    Triglycerides
    Diet Therapy
    Safety
    Hydroxymethylglutaryl-CoA Reductase Inhibitors
    Abdominal Obesity
    Combination Drug Therapy
    Cost-Benefit Analysis
    Insulin Resistance
    Life Style
    Atherosclerosis
    Pharmacology
    Liver
    Therapeutics

    Cite this

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    title = "The metabolic and pharmacologic bases for treating atherogenic dyslipidaemia",
    abstract = "Dyslipoproteinaemia is a cardinal feature of the metabolic syndrome that accelerates atherosclerosis. It is characterized by high plasma concentrations of triglyceride-rich and apolipoprotein (apo) B-containing lipoproteins, with depressed high-density lipoprotein (HDL) and increased small dense low-density lipoprotein (LDL) particle concentrations. Dysregulation of lipoprotein metabolism in the metabolic syndrome may be due to a combination of overproduction of very-low density lipoprotein (VLDL) apoB, decreased catabolism of apoB-containing particles, and increased catabolism of HDL apoA-I particles. These abnormalities are due to a global metabolic effect of insulin resistance and visceral obesity. Lifestyle modifications (dietary restriction and increased exercise) and pharmacological treatments favourably alter lipoprotein transport by decreasing the hepatic secretion of VLDL-apoB and the catabolism of HDL apoA-I, as well as by increasing the clearance of LDL-apoB. The safety and tolerability of combination drug therapy based on statins is important and merits further investigation. There are several pipeline therapies for correcting triglyceride-rich lipoprotein and HDL metabolism. However, their clinical efficacy, safety and cost-effectiveness remain to be demonstrated. {\circledC} 2014 Elsevier Inc. All rights reserved.",
    author = "Dick Chan and Hugh Barrett and Gerald Watts",
    year = "2014",
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    language = "English",
    volume = "28",
    pages = "369--385",
    journal = "Best Practice and Research: Clinical Endocrinology and Metabolism",
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    TY - JOUR

    T1 - The metabolic and pharmacologic bases for treating atherogenic dyslipidaemia

    AU - Chan, Dick

    AU - Barrett, Hugh

    AU - Watts, Gerald

    PY - 2014

    Y1 - 2014

    N2 - Dyslipoproteinaemia is a cardinal feature of the metabolic syndrome that accelerates atherosclerosis. It is characterized by high plasma concentrations of triglyceride-rich and apolipoprotein (apo) B-containing lipoproteins, with depressed high-density lipoprotein (HDL) and increased small dense low-density lipoprotein (LDL) particle concentrations. Dysregulation of lipoprotein metabolism in the metabolic syndrome may be due to a combination of overproduction of very-low density lipoprotein (VLDL) apoB, decreased catabolism of apoB-containing particles, and increased catabolism of HDL apoA-I particles. These abnormalities are due to a global metabolic effect of insulin resistance and visceral obesity. Lifestyle modifications (dietary restriction and increased exercise) and pharmacological treatments favourably alter lipoprotein transport by decreasing the hepatic secretion of VLDL-apoB and the catabolism of HDL apoA-I, as well as by increasing the clearance of LDL-apoB. The safety and tolerability of combination drug therapy based on statins is important and merits further investigation. There are several pipeline therapies for correcting triglyceride-rich lipoprotein and HDL metabolism. However, their clinical efficacy, safety and cost-effectiveness remain to be demonstrated. © 2014 Elsevier Inc. All rights reserved.

    AB - Dyslipoproteinaemia is a cardinal feature of the metabolic syndrome that accelerates atherosclerosis. It is characterized by high plasma concentrations of triglyceride-rich and apolipoprotein (apo) B-containing lipoproteins, with depressed high-density lipoprotein (HDL) and increased small dense low-density lipoprotein (LDL) particle concentrations. Dysregulation of lipoprotein metabolism in the metabolic syndrome may be due to a combination of overproduction of very-low density lipoprotein (VLDL) apoB, decreased catabolism of apoB-containing particles, and increased catabolism of HDL apoA-I particles. These abnormalities are due to a global metabolic effect of insulin resistance and visceral obesity. Lifestyle modifications (dietary restriction and increased exercise) and pharmacological treatments favourably alter lipoprotein transport by decreasing the hepatic secretion of VLDL-apoB and the catabolism of HDL apoA-I, as well as by increasing the clearance of LDL-apoB. The safety and tolerability of combination drug therapy based on statins is important and merits further investigation. There are several pipeline therapies for correcting triglyceride-rich lipoprotein and HDL metabolism. However, their clinical efficacy, safety and cost-effectiveness remain to be demonstrated. © 2014 Elsevier Inc. All rights reserved.

    U2 - 10.1016/j.beem.2013.10.001

    DO - 10.1016/j.beem.2013.10.001

    M3 - Article

    VL - 28

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    EP - 385

    JO - Best Practice and Research: Clinical Endocrinology and Metabolism

    JF - Best Practice and Research: Clinical Endocrinology and Metabolism

    SN - 1521-690X

    IS - 3

    ER -