Peroxisome proliferator-activated receptors are expressed in many tissues, including adipocytes, hepatocytes, muscles and endothelial cells; however, the affinity depends on the isoform of PPAR, and different distribution and expression profiles, which ultimately lead to different clinical outcomes. Because they play an important role in lipid and glucose homeostasis, they are called lipid and insulin sensors. Their actions are limited to specific tissue types and thus, reveal a characteristic influence on target cells. PPARα mainly influences fatty acid metabolism and its activation lowers lipid levels, while PPARγ is mostly involved in the regulation of the adipogenesis, energy balance, and lipid biosynthesis. PPARβ/δ participates in fatty acid oxidation, mostly in skeletal and cardiac muscles, but it also regulates blood glucose and cholesterol levels. Many natural and synthetic ligands influence the expression of these receptors. Synthetic ligands are widely used in the treatment of dyslipidemia (e.g. fibrates - PPARα activators) or in diabetes mellitus (e.g. thiazolidinediones - PPARγ agonists). New generation drugs - PPARα/γ dual agonists - reveal hypolipemic, hypotensive, antiatherogenic, anti-inflammatory and anticoagulant action while the overexpression of PPARβ/δ prevents the development of obesity and reduces lipid accumulation in cardiac cells, even during a high-fat diet. Precise data on the expression and function of natural PPAR agonists on glucose and lipid metabolism are still missing, mostly because the same ligand influences several receptors and a number of reports have provided conflicting results. To date, we know that PPARs have the capability to accommodate and bind a variety of natural and synthetic lipophilic acids, such as essential fatty acids, eicosanoids, phytanic acid and palmitoylethanolamide. A current understanding of the effects of PPARs, their molecular mechanisms and the role of these receptors in nutrition and therapeutic treatment are delineated in this paper.

/pdf/peroxisome-proliferator-activated-receptors-and-their-p0w9f64vqa.pdf

Peroxisome proliferator-activated receptors and their ligands: nutritional and clinical implications - a review

Peroxisome proliferator-activated receptor gamma (PPARγ) has been the focus of intense research because ligands for this receptor have emerged as potent insulin sensitizers used in the treatment of type 2 diabetes. There have been described three PPAR isotypes α, δ and γ which have an integrated role in controlling the expression of genes playing key roles in the storage and mobilization of lipids, in glucose metabolism, in morphogenesis and inflammatory response. Recent advances include the discovery of novel genes that are regulated by PPARγ, which helps to explain how activation of this adipocyte predominant transcription factor regulates glucose and lipid homeostasis. Increased levels of circulating free fatty acids and lipid accumulation in non-adipose tissue have been implicated in the development of insulin resistance. This situation is improved by PPARγ ligands, which promotes fatty acid storage in fat deposits and regulates the expression of adipocyte-secreted hormones that impacts on glucose homeostasis. So the net result of the pleiotropic effects of PPARγ ligands is improvement of insulin sensitivity. This review highlights the roles that PPAR gamma play in the regulation of gene expression of multiple diseases including obesity, diabetes and cancer and highlights the gene isolation transformation role. Further studies are needed for the transformation of PPAR gamma gene in plants and evaluate in animals for the treatment of type 2 diabetes.

PPAR gamma gene – A review

Purpose
To comprehensively review the data on the relationship between the consumption of dairy fat and high-fat dairy foods, obesity, and cardiometabolic disease.

The relationship between high-fat dairy consumption and obesity, cardiovascular, and metabolic disease

Animal models and epidemiological observations suggest that a continuous inflammatory condition predisposes to colorectal cancer (CRC), but the roles of different elements participating in inflammatory responses have been little investigated in relation to CRC. We have studied the association between single nucleotide polymorphisms in the interleukin (IL)-6 (-174 G>C), IL8 (-251T>A), tumor necrosis factor alpha (-308G>A), and PPARG (Pro12Ala) genes and the risk of CRC in a group of 377 cases and 326 controls from Barcelona, Spain. These genes are known to be important for inflammation of the colorectum and common allelic variants have been shown to have a biological effect. The PPARG Ala12 and IL8-251A genotypes are associated with reduced risk of disease (0.56, 95% CI, 0.37-0.85, P = 0.0056, and 0.70, 95% CI, 0.50-0.99, P = 0.043, respectively), whereas the IL6-174C genotype is associated with increased risk (1.53, 95% CI, 1.12-2.09, P = 0.0073). We also studied a single nucleotide polymorphism in intron 11 of the NFKB1 gene (rs1020759), which probably lacks any functional role, and found no significant association with the disease. This is the first report that IL6, IL8, and PPARG genes are important in relation to inflammation-related risk of sporadic CRC.

https://cancerres.aacrjournals.org/content/canres/63/13/3560.full.pdf

Association of common polymorphisms in inflammatory genes interleukin (IL)6, IL8, tumor necrosis factor alpha, NFKB1, and peroxisome proliferator-activated receptor gamma with colorectal cancer.

Prebiotic oligosaccharides modulate the intestinal microbiota and beneficially affect the human body by reducing intestinal inflammation. This immunomodulatory effect was assumed to be bacterial in origin. However, some observations suggest that oligosaccharides may exert an antiinflammatory effect per se. We hypothesized that oligosaccharides affect the intestinal immunity via activation of peptidoglycan recognition protein 3 (PGlyRP3), which reduces the expression of proinflammatory cytokines. Caco-2 cells were treated with the oligosaccharides, α3-sialyllactose, or fructooligosaccharides (Raftilose p95), and the effects of these treatments on PGlyRP3 and PPARγ expression, the release and expression of some proinflammatory cytokines, and NF-κB translocation were tested. Both oligosaccharides had antiinflammatory activity; they significantly reduced IL-12 secretion in Caco-2 cells and gene expression of IL-12p35, IL-8, and TNFα. They also reduced the gene expression and nuclear translocation of NF-κB. Both oligosaccharides dose and time dependently induced the production of PGlyRP3, the silencing of which by transfection of Caco-2 cells with specific small interfering RNA targeting PGlyRP3 abolished the antiinflammatory role of both oligosaccharides. Incubation of Caco-2 cells with both oligosaccharides induced PPARγ. Antagonizing PPARγ by culturing the cells with GW9662 for 24 h inhibited the oligosaccharide-induced PGlyRP3 production and the antiinflammatory effect of the oligosaccharides. We conclude that oligosaccharides may exert an antiinflammatory effect by inducing the nuclear receptor PPARγ, which regulates the antiinflammatory PGlyRP3.

/pdf/prebiotic-oligosaccharides-reduce-proinflammatory-cytokines-1w03yg56e3.pdf

Prebiotic Oligosaccharides Reduce Proinflammatory Cytokines in Intestinal Caco-2 Cells via Activation of PPARγ and Peptidoglycan Recognition Protein 3

SPECIFIC AIMSThe promiscuity of the peroxisome proliferator-activated receptors (PPAR) toward a broad range of exogenous and endogenous ligands suggests a pivotal role between food intake and the transcriptional regulation of glucose and lipid metabolism. In this study, we aimed to identify and elucidate the underling molecular mechanisms of possible beneficial health effects of the natural diet-derived PPAR ligand phytanic acid, with a special emphasis on non-insulin-dependent diabetes mellitus prevention.PRINCIPAL FINDINGS1. Transcriptional activation of PPAR isoforms by phytanic acid in CV-1 cellsWe investigated the trans-activational effect of phytanic acid and its natural stereomers on the acyl CoA oxidase PPAR-responsive element (ACO-PPRE), using a luciferase reporter gene construct (ACO-PPRE)4-tk-luc cotransfected with the human PPAR isoforms α, β, and γ in CV-1 cells. Endogenous ACO gene expression and expression of comparable reporter constructs have been shown to be ligand-dependently activated ...

Phytanic acid, a natural peroxisome proliferator-activated receptor (PPAR) agonist, regulates glucose metabolism in rat primary hepatocytes

Fentanyl is considered to be an effective, transdermal treatment of chronic, cancer, and noncancer pain. This noninterventional, clinical practice-based study, on 426 patients attending 42 practices, assessed a proprietary, Aloe vera-containing, transdermal fentanyl matrix patch (Fentavera), for its analgesic effects, patients' quality of life (QoL) effects, tolerability, and adhesiveness. Study outcomes were mean changes from baseline of patient (11-point scales) and physician (5-point scales) ratings. After 1 and 2 months treatment, there were significant (P 30% at 2 months (response = 2-point decrease on 11-point rating scale). In a large majority of patients, the physicians rated the matrix patch as good or very good for analgesic effect, systemic and local tolerance, and adhesiveness. There were 30 adverse events in 4.2% of patients and analgesic comedications were reduced during treatment compared to before treatment. It is concluded, from this population-based data, that the proprietary, transdermal fentanyl matrix patch is effective and safe for chronic pain management in clinical practice, with significant positive analgesic and QoL effects, while being well tolerated and exhibiting good or very good adhesiveness.

/pdf/noninterventional-study-of-transdermal-fentanyl-fentavera-29ffpq1eu0.pdf

Noninterventional study of transdermal fentanyl (fentavera) matrix patches in chronic pain patients: analgesic and quality of life effects.

Estrogen receptors, members of the nuclear hormone receptor family, are not only able to bind their endogenous hormone, 17β-estradiol, but can also accommodate other naturally-occuring, non-steroidal molecules. Here, we describe a spin-column procedure to determine accurately equilibrium dissociation constants (Kds) and IC50 concentrations for estrogenic compounds. The human wild-type ERα was used to validate the protocol. We expressed the full-length ERα protein in an eukaryotic system to ensure all possible post-transcriptional modifications. The gel filtration-based assay revealed a temperature-dependent Kd shift for ERα. At physiological conditions (150 mM salt, 37°C) we determined the 17β-estradiol Kd for ERα to be 281 ± 13 pmol/L. Positive cooperativity was only apparent at low temperatures and diminished to zero at 37°C. In homologous competition binding experiments using 17β-estradiol, we observed fifty fold higher IC50 values than the respective Kd. This paper presents a reliable and sens...

A spin-column procedure for estrogen receptor equilibrium and competition binding analysis.

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Phytanic acid, a natural peroxisome proliferator-activated receptor (PPAR) agonist, regulates glucose metabolism in rat primary hepatocytes

Noninterventional study of transdermal fentanyl (fentavera) matrix patches in chronic pain patients: analgesic and quality of life effects.

A spin-column procedure for estrogen receptor equilibrium and competition binding analysis.