Peroxisome proliferator-activated receptors (PPARs) in der Gefäßwand – neue Regulatoren der Genexpression in vaskulären Zellen

2001 ◽  
Vol 90 (7) ◽  
pp. 470-477 ◽  
Author(s):  
N. Marx ◽  
V. Hombach
Keyword(s):  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptors

New trends in the pharmacological intervention of PPARs in obesity: Role of natural and synthetic compounds_

2020 ◽  
Vol 28 ◽  
Author(s):  
Seyed Mohammad Nabavi ◽  
Kasi Pandima Devi ◽  
Sethuraman Sathya ◽  
Ana Sanches-Silva ◽  
Listos Joanna ◽  
...  
Keyword(s):  
Tissue Expression ◽  
Health Concern ◽  
Pharmacological Intervention ◽  
Peroxisome Proliferator ◽  
Expression Of Genes ◽  
Ppar Agonists ◽  
Prevalence Of Obesity ◽  
Peroxisome Proliferator Activated Receptors ◽  
Natural And Synthetic

: Obesity is a major health concern for a growing fraction of the population, with the prevalence of obesity and its related metabolic disorders not being fully understood. Over the last decade, many attempts have been undertaken to understand the mechanisms at the basis of this condition, in which the accumulation of fat occurring in adipose tissue, leads to the pathogenesis of obesity related disorders. Among the most recent studies, those on Peroxisome Proliferator Activated Receptors (PPARs) revealed that these nuclear receptor proteins acting as transcription factors, among others, regulate the expression of genes involved in energy, lipid, and glucose metabolisms, and chronic inflammation. The three different isotypes of PPARs, with different tissue expression and ligand binding specificity, exert similar or overlapping functions directly or indirectly linked to obesity. In this study, we reviewed the available scientific reports concerning the PPARs structure and functions, especially in obesity, considering both natural and synthetic ligands and their role in the therapy of obesity and obesity-associated disorders. In the whole, the collected data show that there are both natural and synthetic compounds that show beneficial promising activity as PPAR agonists in chronic diseases related to obesity.

scholarly journals Molecular Mechanisms of Obesity-Linked Cardiac Dysfunction: An Up-Date on Current Knowledge

Cells ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 629
Author(s):  
Jorge Gutiérrez-Cuevas ◽  
Ana Sandoval-Rodriguez ◽  
Alejandra Meza-Rios ◽  
Hugo Christian Monroy-Ramírez ◽  
Marina Galicia-Moreno ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiac Dysfunction ◽  
Molecular Mechanisms ◽  
Current Knowledge ◽  
Peroxisome Proliferator ◽  
White Adipocyte ◽  
Peroxisome Proliferator Activated Receptors ◽  
And Oxidative Stress

Obesity is defined as excessive body fat accumulation, and worldwide obesity has nearly tripled since 1975. Excess of free fatty acids (FFAs) and triglycerides in obese individuals promote ectopic lipid accumulation in the liver, skeletal muscle tissue, and heart, among others, inducing insulin resistance, hypertension, metabolic syndrome, type 2 diabetes (T2D), atherosclerosis, and cardiovascular disease (CVD). These diseases are promoted by visceral white adipocyte tissue (WAT) dysfunction through an increase in pro-inflammatory adipokines, oxidative stress, activation of the renin-angiotensin-aldosterone system (RAAS), and adverse changes in the gut microbiome. In the heart, obesity and T2D induce changes in substrate utilization, tissue metabolism, oxidative stress, and inflammation, leading to myocardial fibrosis and ultimately cardiac dysfunction. Peroxisome proliferator-activated receptors (PPARs) are involved in the regulation of carbohydrate and lipid metabolism, also improve insulin sensitivity, triglyceride levels, inflammation, and oxidative stress. The purpose of this review is to provide an update on the molecular mechanisms involved in obesity-linked CVD pathophysiology, considering pro-inflammatory cytokines, adipokines, and hormones, as well as the role of oxidative stress, inflammation, and PPARs. In addition, cell lines and animal models, biomarkers, gut microbiota dysbiosis, epigenetic modifications, and current therapeutic treatments in CVD associated with obesity are outlined in this paper.

scholarly journals Two antibacterial and PPARα/γ-agonistic unsaturated keto fatty acids from a coral-associated actinomycete of the genus Micrococcus

2020 ◽  
Vol 16 ◽  
pp. 297-304 ◽  
Author(s):  
Amit Raj Sharma ◽  
Enjuro Harunari ◽  
Naoya Oku ◽  
Nobuyasu Matsuura ◽  
Agus Trianto ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Spectroscopic Analysis ◽  
Culture Broth ◽  
Peroxisome Proliferator ◽  
Simulation Studies ◽  
Fish Pathogen ◽  
Chemical Structures ◽  
Agonistic Activity ◽  
Isoform Specificity ◽  
Peroxisome Proliferator Activated Receptors

A pair of geometrically isomeric unsaturated keto fatty acids, (6E,8Z)- and (6E,8E)-5-oxo-6,8-tetradecadienoic acids (1 and 2), were isolated from the culture broth of an actinomycete of the genus Micrococcus, which was associated with a stony coral, Catalaphyllia sp. Their chemical structures were elucidated by spectroscopic analysis including NMR and MS, with special assistance of spin system simulation studies for the assignment of an E geometry at C8 in 2. As metabolites of microbes, compounds 1 and 2 are unprecedented in terms of bearing a 2,4-dienone system. Both 1 and 2 showed antibacterial activity against the plant pathogen Rhizobium radiobacter and the fish pathogen Tenacibaculum maritimum, with a contrasting preference that 1 is more effective to the former strain while 2 is so to the latter. In addition, compounds 1 and 2 displayed agonistic activity against peroxisome proliferator-activated receptors (PPARs) with an isoform specificity towards PPARα and PPARγ.

scholarly journals Molecular Recognition of Fatty Acids by Peroxisome Proliferator–Activated Receptors

1999 ◽  
Vol 3 (3) ◽  
pp. 397-403 ◽  
Author(s):  
H.Eric Xu ◽  
Millard H Lambert ◽  
Valerie G Montana ◽  
Derek J Parks ◽  
Steven G Blanchard ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Molecular Recognition ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptors

Peroxisome Proliferator-Activated Receptors and Lipid Metabolism

1993 ◽  
Vol 684 (1 Zinc-Finger P) ◽  
pp. 157-173 ◽  
Author(s):  
HANSJÖRG KELLER ◽  
ABDERRAHIM MAHFOUDI ◽  
CHRISTINE DREYER ◽  
ABDELMADJID K. HIHI ◽  
JEFFREY MEDIN ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptors

scholarly journals PPAR-γImpairment Alters Peroxisome Functionality in Primary Astrocyte Cell Cultures

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Lorenzo Di Cesare Mannelli ◽  
Matteo Zanardelli ◽  
Laura Micheli ◽  
Carla Ghelardini
Keyword(s):  
Antioxidant Defenses ◽  
Nadh:Ubiquinone Oxidoreductase ◽  
Peroxisome Proliferator ◽  
Defense Enzyme ◽  
Primary Astrocyte ◽  
Antioxidant Defense Enzyme ◽  
Rat Astrocytes ◽  
Series Of Experiments ◽  
Peroxisome Proliferator Activated Receptors ◽  
Acyl Coenzyme A

Peroxisomes provide glial cells with protective functions against the harmful effects of H2O2on neurons and peroxisome impairment results in nervous lesions. Agonists of theγ-subtype of the Peroxisome-Proliferator-Activated-Receptors (PPAR) have been proposed as neuroprotective agents in neurodegenerative disorders. Nevertheless, the role of PPAR-γalterations in pathophysiological mechanisms and the relevance of peroxisome functions in the PPAR-γeffects are not yet clear. In a primary cell culture of rat astrocytes, the irreversible PPAR-γantagonist GW9662 concentration-dependently decreased the activity of catalase, the most important antioxidant defense enzyme in peroxisomes. Catalase functionality recovered in a few days and the PPAR-γagonist rosiglitazone promoted reversal of enzymatic damage. The reversible antagonist G3335 reduced both the activity and expression of catalase in a rosiglitazone-prevented manner. G3335 reduced also the glutathione reductase expression, indicating that enzyme involved in glutathione regeneration was compromised. Neither the PPAR-αtarget gene Acyl-Coenzyme-A-oxidase-1 nor the mitochondrial detoxifying enzyme NADH:ubiquinone-oxidoreductase (NDFUS3) was altered by PPAR-γinhibition. In conclusion, PPAR-γinhibition induced impairment of catalase in astrocytes. A general decrease of the antioxidant defenses of the cell suggests that a PPAR-γhypofunction could participate in neurodegenerative mechanisms through peroxisomal damage. This series of experiments could be a useful model for studying compounds able to restore peroxisome functionality.

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