Peroxisome proliferators are non-genotoxic carcinogens which are purported to exert their effect on cells by interacting with members of the nuclear hormone receptor superfamily known as peroxisome proliferator activated receptors (PPARs). There are four of these nuclear hormone receptors known to date, and they are ligand-dependent intracellular proteins that stimulate downstream gene transcription of genes such as acyl coenzyme A oxidase and cytochrome P450 (CYP450). Activation occurs through direct binding to specific DNA response elements following activation by an appropriate ligand. PPARs have pleiotropic effects upon a wide range of cellular functions including vascular tone, inflammation and energy homeostasis. Because of this, PPARs are important targets to consider in therapies for hypertension, obesity, and metabolic syndromes.
PPAR gamma in particular has been of particular interest because its ligands are potent insulin sensitizers for the treatment and management of type 2 diabetes. A recent review on the role of PPARs in hypertension was published by Usuda et al where they summarized the different isoform characteristics, as well as review the experimental and clinical evidence on PPAR agonists in treating lifestyle-related diseases (1). Furthermore, in another very recent publication, Janani et al presented a fairly comprehensive review specifically focused on PPAR gamma modulation of gene expression in multiple diseases such as obesity, diabetes, and cancer (2). Another recent review from Pawlak focuses on the role of the PPAR family on lipid metabolism, inflammation, and fibrosis in non-alcoholic liver disease (3). Lutay et al from Lund University performed immunoblotting with the PPAR gamma antibody to demonstrate that mycobacteria induce an epithelial anti-inflammatory IL-22 and IL-10 response through suppression of NFkB signaling (4). Furthermore, Mattace Raso’s group used the PPAR gamma antibody to monitor the protective effects of sodium butyrate and derivatives on liver inflammation, stenosis, and glucose tolerance in a chronic liver disease rat animal model (5). Their results suggest that butyrate is effective against insulin resistance (IR) and requires further investigation.
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