scholarly journals Peroxisome proliferator-activated receptors, metabolic syndrome and cardiovascular disease

2010 ◽  
Vol 6 (5) ◽  
pp. 657-691 ◽  
Author(s):  
Salman Azhar
Keyword(s):  
Cardiovascular Disease ◽  
Metabolic Syndrome ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptors

scholarly journals Genetic Polymorphisms in the HTR2C and Peroxisome Proliferator-Activated Receptors Are Not Associated with Metabolic Syndrome in Patients with Schizophrenia Taking Clozapine

2011 ◽  
Vol 8 (3) ◽  
pp. 262 ◽  
Author(s):  
Shi Hyun Kang ◽  
Jong Il Lee ◽  
An Kee Chang ◽  
Yeon Ho Joo ◽  
Chang Yoon Kim ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Genetic Polymorphisms ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptors

scholarly journals Screening of Peroxisome Proliferator-activated Receptors (PPARs) α, γ and δ Gene Polymorphisms for Obesity and Metabolic Syndrome Association in the Multi-ethnic Malaysian Population

2015 ◽  
Vol 25 (4) ◽  
pp. 383 ◽  
Author(s):  
Phee-Phee Chia ◽  
Sook-Ha Fan ◽  
Yee-How Say
Keyword(s):  
Metabolic Syndrome ◽  
Demographic Data ◽  
Plasma Lipid ◽  
Peroxisome Proliferator ◽  
Nucleotide Polymorphisms ◽  
Ethnic Population ◽  
Single Nucleotide ◽  
Peroxisome Proliferator Activated Receptor ◽  
Ethnic Chinese ◽  
Peroxisome Proliferator Activated Receptors

<p class="Pa7"><strong>Objective: </strong>This study aimed to investigate the association of peroxisome proliferator-activated receptor (PPAR) genes <em>PPAR</em>α L162V, <em>PPAR</em><em>γ</em><em>2 </em>C161T and <em>PPAR</em><em>δ </em>T294C single nucleotide polymorphisms (SNPs) with obesity and metabolic syndrome (Met- S) in a multi-ethnic population in Kampar, Malaysia.</p><p class="Pa7"><strong>Methods: </strong>Socio-demographic data, anthropometric and biochemical measure­ments (plasma lipid profile, adiponectin and interleukin-6 [IL-6] levels) were taken from 307 participants (124 males; 180 obese; 249 Met-S; 97 Malays, 85 ethnic Chinese, 55 ethnic Indians).</p><p class="Pa7"><strong>Results: </strong>The overall minor allele frequen­cies were .08, .22 and .30 for <em>PPAR </em>α L162V, γ C161T, δ T294C, respectively. All SNPs were not associated with obesity, Met-S and obesity with/without Met-S by χ2 analysis, ethnicity-stratified and logistic re­gression analyses. Nevertheless, participants with V162 allele of <em>PPAR</em><em>α </em>had significantly higher IL-6, while those with T161 allele of <em>PPAR</em><em>γ</em><em>2 </em>had significantly lower HOMA-IR.</p><p><strong>Conclusions: </strong>All <em>PPAR </em>SNPs were not associated with obesity and Met-S in the suburban population of Kampar, Malay­sia, where only <em>PPAR</em><em>α </em>V162 and <em>PPAR</em><em>γ</em><em>2 </em>T161 alleles were associated with plasma IL-6 and HOMA-IR, respectively. <em>Ethn Dis. </em>2015;25(4):383-390; doi:10.18865/ ed.25.4.383</p>

Peroxisome proliferator-activated receptors and cardiovascular remodeling

2005 ◽  
Vol 288 (3) ◽  
pp. H1037-H1043 ◽  
Author(s):  
Ernesto L. Schiffrin
Keyword(s):  
Cardiovascular Disease ◽  
Target Genes ◽  
Acid Oxidation ◽  
Peroxisome Proliferator ◽  
Fat Cell ◽  
Ppar Γ ◽  
Peroxisome Proliferator Activated Receptors ◽  
Prevention Of Cardiovascular Disease

Peroxisome proliferator-activated receptors (PPARs) are nuclear receptors that heterodimerize with the retinoid X receptor and then modulate the function of many target genes. Three PPARs are known: α, β/δ, and γ. The better known are PPAR-α and PPAR-γ, which may be activated by different synthetic agonists, although the endogenous ligands are unknown. PPAR-α is involved in fatty acid oxidation and expressed in the liver, kidney, and skeletal muscle, whereas PPAR-γ is involved in fat cell differentiation, lipid storage, and insulin sensitivity. However, both have been shown to be present in variable amounts in cardiovascular tissues, including endothelium, smooth muscle cells, macrophages, and the heart. The activators of PPAR-α (fibrates) and PPAR-γ (thiazolidinediones or glitazones) antagonized the actions of angiotensin II in vivo and in vitro and exerted cardiovascular antioxidant and anti-inflammatory effects. PPAR activators lowered blood pressure, induced favorable effects on the heart, and corrected vascular structure and endothelial dysfunction in several rodent models of hypertension. Activators of PPARs may become therapeutic agents useful in the prevention of cardiovascular disease beyond their effects on carbohydrate and lipid metabolism. Some side effects, such as weight gain, as well as documented aggravation of advanced heart failure through fluid retention by glitazones, may, however, limit their therapeutic application in prevention of cardiovascular disease.

scholarly journals Resveratrol and Quercetin as Regulators of Inflammatory and Purinergic Receptors to Attenuate Liver Damage Associated to Metabolic Syndrome

2021 ◽  
Vol 22 (16) ◽  
pp. 8939
Author(s):  
Agustina Cano-Martínez ◽  
Rocío Bautista-Pérez ◽  
Vicente Castrejón-Téllez ◽  
Elizabeth Carreón-Torres ◽  
Israel Pérez-Torres ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Liver Damage ◽  
Purinergic Receptor ◽  
Critical Role ◽  
Hepatocyte Proliferation ◽  
Peroxisome Proliferator ◽  
Ppar Alpha ◽  
Nonalcoholic Fatty Liver ◽  
Beneficial Effects ◽  
Peroxisome Proliferator Activated Receptors

Nonalcoholic fatty liver disease (NAFLD) is considered a manifestation of metabolic syndrome (MS) and is characterized by the accumulation of triglycerides and a varying degree of hepatic injury, inflammation, and repair. Moreover, peroxisome-proliferator-activated receptors (PPARs) play a critical role in the pathophysiological processes in the liver. There is extensive evidence of the beneficial effect of polyphenols such as resveratrol (RSV) and quercetin (QRC) on the treatment of liver pathology; however, the mechanisms underlying their beneficial effects have not been fully elucidated. In this work, we show that the mechanisms underlying the beneficial effects of RSV and QRC against inflammation in liver damage in our MS model are due to the activation of novel pathways which have not been previously described such as the downregulation of the expression of toll-like receptor 4 (TLR4), neutrophil elastase (NE) and purinergic receptor P2Y2. This downregulation leads to a decrease in apoptosis and hepatic fibrosis with no changes in hepatocyte proliferation. In addition, PPAR alpha and gamma expression were altered in MS but their expression was not affected by the treatment with the natural compounds. The improvement of liver damage by the administration of polyphenols was reflected in the normalization of serum transaminase activities.

scholarly journals Peroxisome Proliferator-Activated Receptors - Alpha in Chronic Inflammation - Mini-Review

2019 ◽  
Vol 12 ◽  
pp. 1-11
Author(s):  
Elena Popa ◽  
Florin Zugun-Eloae ◽  
Mihaela Zlei ◽  
Maria Traian ◽  
Agnes Bacusca ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Transcription Factors ◽  
Lipid Metabolism ◽  
Visceral Obesity ◽  
Peroxisome Proliferator ◽  
Proinflammatory Response ◽  
The Metabolic Syndrome ◽  
Metabolic Complication ◽  
Peroxisome Proliferator Activated Receptors ◽  
Proinflammatory Factors

The pathogeny of the metabolic syndrome (MetS ) is not fully elucidated, but a link between visceral obesity and the increase of the proinflammatory response was proven. Atherosclerosis, perceived as a metabolic complication, draws attention to the peroxisome proliferator-activated receptors- alpha (PPARα). PPARα receptors are transcription factors involved in lipid metabolism, inflammation and atheromatosis. Hence, it interferes in the pathogeny of cardiovascular diseases and other chronic diseases too (neurological, psychical, neoplasical). The study of the expression of PPARα and its modulation on different level may be beneficial in the treatment of metabolic syndrome, intervening in the modulation of another proinflammatory factors.

scholarly journals Trace Elements, PPARs, and Metabolic Syndrome

2020 ◽  
Vol 21 (7) ◽  
pp. 2612 ◽  
Author(s):  
Yujie Shi ◽  
Yixin Zou ◽  
Ziyue Shen ◽  
Yonghong Xiong ◽  
Wenxiang Zhang ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Trace Elements ◽  
Mrna Expression ◽  
High Fat Diet ◽  
Binding Activity ◽  
Peroxisome Proliferator ◽  
Dna Binding Activity ◽  
Ppar Γ ◽  
Peroxisome Proliferator Activated Receptors ◽  
Structure Of Proteins

Metabolic syndrome (MetS) is a constellation of metabolic derangements, including central obesity, insulin resistance, hypertension, glucose intolerance, and dyslipidemia. The pathogenesis of MetS has been intensively studied, and now many factors are recognized to contribute to the development of MetS. Among these, trace elements influence the structure of proteins, enzymes, and complex carbohydrates, and thus an imbalance in trace elements is an independent risk factor for MetS. The molecular link between trace elements and metabolic homeostasis has been established, and peroxisome proliferator-activated receptors (PPARs) have appeared as key regulators bridging these two elements. This is because on one hand, PPARs are actively involved in various metabolic processes, such as abdominal adiposity and insulin sensitivity, and on the other hand, PPARs sensitively respond to changes in trace elements. For example, an iron overload attenuates hepatic mRNA expression of Ppar-α; zinc supplementation is considered to recover the DNA-binding activity of PPAR-α, which is impaired in steatotic mouse liver; selenium administration downregulates mRNA expression of Ppar-γ, thereby improving lipid metabolism and oxidative status in the liver of high-fat diet (HFD)-fed mice. More importantly, PPARs’ expression and activity are under the control of the circadian clock and show a robust 24 h rhythmicity, which might be the reasons for the side effects and the clinical limitations of trace elements targeting PPARs. Taken together, understanding the casual relationships among trace elements, PPARs’ actions, and the pathogenesis of MetS is of great importance. Further studies are required to explore the chronopharmacological effects of trace elements on the diurnal oscillation of PPARs and the consequent development of MetS.

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