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Free fatty acids may be involved in the pathogenesis of oral-related and cardiovascular diseases

Y. Shikama

Published 2018 in Journal of Oral Biosciences

ABSTRACT

Abstract Background Adipose tissue insulin resistance plays an important role in the development of type 2 diabetes (T2D) and is characterized by a high rate of lipolysis, resulting in increased plasma free fatty acid (FFA) levels. Among various FFAs, saturated fatty acids (SFAs), such as palmitate (Pal) and stearate, can induce inflammatory responses. Moreover, CD36 (involved in FFA uptake) and its ligands can promote sterile inflammation through the assembly of Toll-like receptor heterodimers. The involvement of these molecules and receptors in the pathogenesis of both oral-related and cardiovascular diseases has been demonstrated. Highlight SFAs but not unsaturated fatty acids could induce interleukin (IL)-6 production, apoptosis, and α-fodrin degradation in the salivary gland epithelial cells of patients with primary Sjogren's syndrome. High-fat-diet-induced T2D model mice were demonstrated to have a higher expression of CD36 on the surface of gingival fibroblasts. Pal could induce interleukin (IL)-6, IL-8, and CXCL1 secretion in human gingival fibroblasts (HGFs). Porphyromonas gingivalis ( P. gingivalis ) lipopolysaccharide (LPS) and heat-killed P. gingivalis could augment Pal-induced chemokine secretion in HGFs. Moreover, SFAs were found to increase IL-1β secretion and decrease IL-1 receptor antagonist (IL-1Ra) secretion in human monocytes, resulting in an increase in the IL-1β/IL-1Ra secretion ratio. This could induce the expression and release of adhesion molecules, such as intercellular adhesion molecule-1 (ICAM-1) and E-selectin, in human aortic and vein endothelial cells. Conclusion In this review, we summarize a potential link between FFAs and the pathogenesis of craniofacial and cardiovascular diseases.

PUBLICATION RECORD

  • Publication year

    2018

  • Venue

    Journal of Oral Biosciences

  • Publication date

    2018-09-01

  • Fields of study

    Biology, Medicine, Chemistry, Environmental Science

  • Identifiers
    DOI 10.1016/J.JOB.2018.04.001
  • External record

    Open on Semantic Scholar

  • Source metadata

    Semantic Scholar

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