Dyslipidemia in Obesity

    Research output: Chapter in Book/Conference paperChapter

    Abstract

    Obesity is associated with an increased risk of atherosclerosis and coronary artery disease, in part due to its strong association with atherogenic dyslipidemia. The latter is characterized by elevated plasma triglycerides, low plasma high-density lipoprotein (HDL) cholesterol, and high plasma concentrations of apolipoprotein (apo) B-containing lipoproteins. Dysregulation of lipoprotein metabolism in obese subjects may be due to a combination of overproduction of very-low-density lipoprotein, decreased catabolism of apoB-containing particles, and increased catabolism of HDL particles. These abnormalities may be consequent on a global metabolic effect of insulin resistance and an excess of visceral fat. Lifestyle modifications (dietary restriction and increased physical activity) are first-line therapies to improve lipid abnormalities in obesity. Pharmacological treatments, such as statins, fibrates, ezetimibe, and fish oils, could also be employed alone or in combination with other agents to optimize the benefit of lifestyle modifications on atherogenic dyslipidemia. Kinetic studies show that improvements in lipid and lipoprotein profiles in obesity can be collectively achieved by several mechanisms of action including decreased secretion and increased catabolism of apoB, as well as increased secretion and decreased catabolism of apoA-I. There are several pipeline therapies for correcting atherogenic abnormalities in lipoprotein metabolism. However, their clinical efficacy, safety, and cost-effectiveness remain to be demonstrated.
    Original languageEnglish
    Title of host publicationMetabolic Syndrome: A Comprehensive Textbook
    EditorsRexford S. Ahima
    Place of PublicationCham
    PublisherSpringer International Publishing
    Pages525-540
    ISBN (Print)9783319121253
    DOIs
    Publication statusPublished - 2015

    Fingerprint

    Dyslipidemias
    Obesity
    Lipoproteins
    Apolipoproteins B
    Life Style
    Diet Therapy
    Lipids
    Fibric Acids
    Hydroxymethylglutaryl-CoA Reductase Inhibitors
    Intra-Abdominal Fat
    VLDL Lipoproteins
    Fish Oils
    Apolipoprotein A-I
    HDL Lipoproteins
    HDL Cholesterol
    Cost-Benefit Analysis
    Insulin Resistance
    Coronary Artery Disease
    Atherosclerosis
    Triglycerides

    Cite this

    Chan, D. C., Pang, J., & Watts, G. F. (2015). Dyslipidemia in Obesity. In R. S. Ahima (Ed.), Metabolic Syndrome: A Comprehensive Textbook (pp. 525-540). Cham: Springer International Publishing. https://doi.org/10.1007/978-3-319-12125-3_30-1
    Chan, Dick C. ; Pang, Jing ; Watts, Gerald F. / Dyslipidemia in Obesity. Metabolic Syndrome: A Comprehensive Textbook. editor / Rexford S. Ahima. Cham : Springer International Publishing, 2015. pp. 525-540
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    abstract = "Obesity is associated with an increased risk of atherosclerosis and coronary artery disease, in part due to its strong association with atherogenic dyslipidemia. The latter is characterized by elevated plasma triglycerides, low plasma high-density lipoprotein (HDL) cholesterol, and high plasma concentrations of apolipoprotein (apo) B-containing lipoproteins. Dysregulation of lipoprotein metabolism in obese subjects may be due to a combination of overproduction of very-low-density lipoprotein, decreased catabolism of apoB-containing particles, and increased catabolism of HDL particles. These abnormalities may be consequent on a global metabolic effect of insulin resistance and an excess of visceral fat. Lifestyle modifications (dietary restriction and increased physical activity) are first-line therapies to improve lipid abnormalities in obesity. Pharmacological treatments, such as statins, fibrates, ezetimibe, and fish oils, could also be employed alone or in combination with other agents to optimize the benefit of lifestyle modifications on atherogenic dyslipidemia. Kinetic studies show that improvements in lipid and lipoprotein profiles in obesity can be collectively achieved by several mechanisms of action including decreased secretion and increased catabolism of apoB, as well as increased secretion and decreased catabolism of apoA-I. There are several pipeline therapies for correcting atherogenic abnormalities in lipoprotein metabolism. However, their clinical efficacy, safety, and cost-effectiveness remain to be demonstrated.",
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    Chan, DC, Pang, J & Watts, GF 2015, Dyslipidemia in Obesity. in RS Ahima (ed.), Metabolic Syndrome: A Comprehensive Textbook. Springer International Publishing, Cham, pp. 525-540. https://doi.org/10.1007/978-3-319-12125-3_30-1

    Dyslipidemia in Obesity. / Chan, Dick C.; Pang, Jing; Watts, Gerald F.

    Metabolic Syndrome: A Comprehensive Textbook. ed. / Rexford S. Ahima. Cham : Springer International Publishing, 2015. p. 525-540.

    Research output: Chapter in Book/Conference paperChapter

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    N2 - Obesity is associated with an increased risk of atherosclerosis and coronary artery disease, in part due to its strong association with atherogenic dyslipidemia. The latter is characterized by elevated plasma triglycerides, low plasma high-density lipoprotein (HDL) cholesterol, and high plasma concentrations of apolipoprotein (apo) B-containing lipoproteins. Dysregulation of lipoprotein metabolism in obese subjects may be due to a combination of overproduction of very-low-density lipoprotein, decreased catabolism of apoB-containing particles, and increased catabolism of HDL particles. These abnormalities may be consequent on a global metabolic effect of insulin resistance and an excess of visceral fat. Lifestyle modifications (dietary restriction and increased physical activity) are first-line therapies to improve lipid abnormalities in obesity. Pharmacological treatments, such as statins, fibrates, ezetimibe, and fish oils, could also be employed alone or in combination with other agents to optimize the benefit of lifestyle modifications on atherogenic dyslipidemia. Kinetic studies show that improvements in lipid and lipoprotein profiles in obesity can be collectively achieved by several mechanisms of action including decreased secretion and increased catabolism of apoB, as well as increased secretion and decreased catabolism of apoA-I. There are several pipeline therapies for correcting atherogenic abnormalities in lipoprotein metabolism. However, their clinical efficacy, safety, and cost-effectiveness remain to be demonstrated.

    AB - Obesity is associated with an increased risk of atherosclerosis and coronary artery disease, in part due to its strong association with atherogenic dyslipidemia. The latter is characterized by elevated plasma triglycerides, low plasma high-density lipoprotein (HDL) cholesterol, and high plasma concentrations of apolipoprotein (apo) B-containing lipoproteins. Dysregulation of lipoprotein metabolism in obese subjects may be due to a combination of overproduction of very-low-density lipoprotein, decreased catabolism of apoB-containing particles, and increased catabolism of HDL particles. These abnormalities may be consequent on a global metabolic effect of insulin resistance and an excess of visceral fat. Lifestyle modifications (dietary restriction and increased physical activity) are first-line therapies to improve lipid abnormalities in obesity. Pharmacological treatments, such as statins, fibrates, ezetimibe, and fish oils, could also be employed alone or in combination with other agents to optimize the benefit of lifestyle modifications on atherogenic dyslipidemia. Kinetic studies show that improvements in lipid and lipoprotein profiles in obesity can be collectively achieved by several mechanisms of action including decreased secretion and increased catabolism of apoB, as well as increased secretion and decreased catabolism of apoA-I. There are several pipeline therapies for correcting atherogenic abnormalities in lipoprotein metabolism. However, their clinical efficacy, safety, and cost-effectiveness remain to be demonstrated.

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    Chan DC, Pang J, Watts GF. Dyslipidemia in Obesity. In Ahima RS, editor, Metabolic Syndrome: A Comprehensive Textbook. Cham: Springer International Publishing. 2015. p. 525-540 https://doi.org/10.1007/978-3-319-12125-3_30-1