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Trans fatty acids - effects on systemic inflammation and endothelial function.

Abstract

Consumption of trans fatty acids (TFA) predicts higher risk of coronary heart disease, sudden death, and possibly diabetes mellitus. These associations are greater than would be predicted by effects of TFA on serum lipoproteins alone. Systemic inflammation and endothelial dysfunction may be involved in the pathogenesis of atherosclerosis, acute coronary syndromes, sudden death, insulin resistance, dyslipidemia, and heart failure. Evidence from both observational and experimental studies indicates that TFA are pro-inflammatory. Limited evidence suggests that pro-inflammatory effects may be stronger for trans isomers of linoleic acid (trans-C18:2) and oleic acid (trans-C18:1), rather than of palmitoleic acid (trans-C16:1), but further study of potential isomer-specific effects is needed. TFA also appear to induce endothelial dysfunction. The mechanisms underlying these effects are not well-established, but may involve TFA incorporation into endothelial cell, monocyte/macrophage, or adipocyte cell membranes (affecting membrane signaling pathway relating to inflammation) or ligand-dependent effects on peroxisome proliferator-activated receptor (PPAR) or retinoid X receptor (RXR) pathways. Activation of inflammatory responses and endothelial dysfunction may represent important mediating pathways between TFA consumption and risk of coronary heart disease, sudden death, and diabetes. Further study is indicated to define these effects of TFA and the implications of such effects for cardiovascular health.

Links

  • Publisher Full Text
  • Authors+Show Affiliations

    The Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA. dmozaffa@hsph.harvard.edu

    Source

    Atherosclerosis. Supplements 7:2 2006 May pg 29-32

    MeSH

    Atherosclerosis
    Coronary Disease
    Dietary Fats, Unsaturated
    Endothelium, Vascular
    Humans
    Inflammation
    Peroxisome Proliferator-Activated Receptors
    Retinoid X Receptors
    Signal Transduction
    Trans Fatty Acids

    Pub Type(s)

    Journal Article
    Research Support, N.I.H., Extramural
    Review

    Language

    eng

    PubMed ID

    16713393

    Citation

    Mozaffarian, Dariush. "Trans Fatty Acids - Effects On Systemic Inflammation and Endothelial Function." Atherosclerosis. Supplements, vol. 7, no. 2, 2006, pp. 29-32.
    Mozaffarian D. Trans fatty acids - effects on systemic inflammation and endothelial function. Atheroscler Suppl. 2006;7(2):29-32.
    Mozaffarian, D. (2006). Trans fatty acids - effects on systemic inflammation and endothelial function. Atherosclerosis. Supplements, 7(2), pp. 29-32.
    Mozaffarian D. Trans Fatty Acids - Effects On Systemic Inflammation and Endothelial Function. Atheroscler Suppl. 2006;7(2):29-32. PubMed PMID: 16713393.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Trans fatty acids - effects on systemic inflammation and endothelial function. A1 - Mozaffarian,Dariush, Y1 - 2006/05/18/ PY - 2006/5/23/pubmed PY - 2006/11/15/medline PY - 2006/5/23/entrez SP - 29 EP - 32 JF - Atherosclerosis. Supplements JO - Atheroscler Suppl VL - 7 IS - 2 N2 - Consumption of trans fatty acids (TFA) predicts higher risk of coronary heart disease, sudden death, and possibly diabetes mellitus. These associations are greater than would be predicted by effects of TFA on serum lipoproteins alone. Systemic inflammation and endothelial dysfunction may be involved in the pathogenesis of atherosclerosis, acute coronary syndromes, sudden death, insulin resistance, dyslipidemia, and heart failure. Evidence from both observational and experimental studies indicates that TFA are pro-inflammatory. Limited evidence suggests that pro-inflammatory effects may be stronger for trans isomers of linoleic acid (trans-C18:2) and oleic acid (trans-C18:1), rather than of palmitoleic acid (trans-C16:1), but further study of potential isomer-specific effects is needed. TFA also appear to induce endothelial dysfunction. The mechanisms underlying these effects are not well-established, but may involve TFA incorporation into endothelial cell, monocyte/macrophage, or adipocyte cell membranes (affecting membrane signaling pathway relating to inflammation) or ligand-dependent effects on peroxisome proliferator-activated receptor (PPAR) or retinoid X receptor (RXR) pathways. Activation of inflammatory responses and endothelial dysfunction may represent important mediating pathways between TFA consumption and risk of coronary heart disease, sudden death, and diabetes. Further study is indicated to define these effects of TFA and the implications of such effects for cardiovascular health. SN - 1567-5688 UR - https://www.unboundmedicine.com/medline/citation/16713393/full_citation L2 - https://linkinghub.elsevier.com/retrieve/pii/S1567-5688(06)00032-8 DB - PRIME DP - Unbound Medicine ER -