The relationship of lipid imbalance and chronic inflammation mediated by PPAR

Obesity is a serious metabolic disease that threatens patients with increasing incidence of the metabolic, cardiovascular, cancer^1-3) 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 tissue^{5, 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.

Keywords: obesity; inflammation; PPAR-γ; cytokines

Grants and funding:

Článok vznikol vďaka podpore v rámci OP Výskum a vývoj pre dopytovo-orientovaný projekt: Univerzitný vedecký park Univerzity Komenského v Bratislave, ITMS 26240220086 spolufinancovaný zo zdrojov Európskeho fondu regionálneho rozvoja a grantu FaF UK/12/2015.