The relationship of lipid imbalance and chronic inflammation mediated by PPAR

Authors: Tomáš Čavojský;  František Bilka;  Ingrid Pauliková
Published in: Čes. slov. Farm., 2016; 65, 3-9
Category: Review Articles


Obesity is a serious metabolic disease that threatens patients with increasing incidence of the metabolic, cardiovascular, cancer1–3) and other associated, especially autoimmune diseases. It increases significantly the morbidity and mortality of patients and reduces quality of their life.

The imbalance between lipolysis and lipogenesis results in a number of metabolic related disorders at the different regulatory levels of transcription, translation, and/or activity of enzymes. One of the extensively studied areas in regulating lipogenesis, often accompanied by inflammation, is a peroxisome proliferator activated receptors (PPARs), especially its isomer PPAR-γ. PPAR-γ is a ligand-activated transcription factor belonging to the family of nuclear receptors. It is mostly presented in differentiated macrophages and adipose tissue5, 6). It has an important function of adipocyte differentiation and inflammation management in terms of gene expression inhibition of pro-inflammatory cytokines. PPAR-γ inhibition of inflammatory cytokines such as TNF-α may present the molecular mechanism of lipid disorders, thus contributing to the pathogenesis of various diseases, e.g. inflammation, insulin resistance and atherosclerosis, for which the lipid metabolism disorders are a common feature. Under the action of specific agonists, PPAR-γ alter the release of signal molecules from adipose tissue, which has far-reaching metabolic consequences in other tissues. It plays an important role in the inhibition of inflammation and the development of insulin resistance.

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