scholarly journals The potential pathways underlying the association of propyl-paraben exposure with aeroallergen sensitization and EASI score using metabolomics analysis

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yujin Lee ◽  
Eun Lee ◽  
Dong Keon Yon ◽  
Hye Mi Jee ◽  
Hey Sung Baek ◽  
...  
Keyword(s):  
Tricarboxylic Acid Cycle ◽  
Picolinic Acid ◽  
Severity Index ◽  
Untargeted Metabolomics ◽  
Peroxisome Proliferator ◽  
General Population Study ◽  
Propyl Paraben ◽  
Aryl Hydrocarbon ◽  
Peroxisome Proliferator Activated Receptors ◽  
Metabolomics Analysis

AbstractPropyl-paraben exposure is associated with aeroallergen sensitization, but its association with atopic dermatitis (AD) is inconclusive. No studies have been conducted on the metabolomic pathways underlying these associations. We investigated the associations between propyl-paraben exposure and aeroallergen sensitization, AD, and Eczema Area and Severity Index (EASI) score and identified the underlying pathways using untargeted metabolomics analysis. We enrolled 455 children in a general population study. Skin prick tests were performed with the assessment of EASI score. Urinary propyl-, butyl-, ethyl-, and methyl-paraben levels were measured. Untargeted metabolomics analysis was performed on the first and fifth urine propyl-paraben quintile groups. The highest urine propyl-paraben quintile group was associated with aeroallergen sensitization, but not with AD. Glycine, threonine, serine, ornithine, isoleucine, arabinofuranose, d-lyxofuranose, citrate, and picolinic acid levels were higher, whereas palmitic acid and 2-palmitoylglycerol levels were lower in the highest quintile propyl-paraben group, than in the lowest quintile group. The propyl-paraben-induced metabolic perturbations were associated with serine and glycine metabolisms, branched-chain amino acid metabolism, and ammonia recycling. Propyl-paraben exposure was associated with aeroallergen sensitization and EASI score, partially via metabolomic changes related with oxidative stress, mTOR, peroxisome proliferator-activated receptors pathway, aryl hydrocarbon receptor signaling pathways, and tricarboxylic acid cycle.

scholarly journals Nuclear Receptors in Myocardial and Cerebral Ischemia—Mechanisms of Action and Therapeutic Strategies

2021 ◽  
Vol 22 (22) ◽  
pp. 12326
Author(s):  
Joanna Rzemieniec ◽  
Laura Castiglioni ◽  
Paolo Gelosa ◽  
Majeda Muluhie ◽  
Benedetta Mercuriali ◽  
...  
Keyword(s):  
Cardiovascular Diseases ◽  
Nuclear Receptors ◽  
Mechanisms Of Action ◽  
Experimental Models ◽  
Therapeutic Window ◽  
Peroxisome Proliferator ◽  
Aryl Hydrocarbon ◽  
Heart Ischemia ◽  
Peroxisome Proliferator Activated Receptors ◽  
The Brain

Nearly 18 million people died from cardiovascular diseases in 2019, of these 85% were due to heart attack and stroke. The available therapies although efficacious, have narrow therapeutic window and long list of contraindications. Therefore, there is still an urgent need to find novel molecular targets that could protect the brain and heart against ischemia without evoking major side effects. Nuclear receptors are one of the promising targets for anti-ischemic drugs. Modulation of estrogen receptors (ERs) and peroxisome proliferator-activated receptors (PPARs) by their ligands is known to exert neuro-, and cardioprotective effects through anti-apoptotic, anti-inflammatory or anti-oxidant action. Recently, it has been shown that the expression of aryl hydrocarbon receptor (AhR) is strongly increased after brain or heart ischemia and evokes an activation of apoptosis or inflammation in injury site. We hypothesize that activation of ERs and PPARs and inhibition of AhR signaling pathways could be a promising strategy to protect the heart and the brain against ischemia. In this Review, we will discuss currently available knowledge on the mechanisms of action of ERs, PPARs and AhR in experimental models of stroke and myocardial infarction and future perspectives to use them as novel targets in cardiovascular diseases.

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 Quick-start infrastructure for untargeted metabolomics analysis in GNPS

2021 ◽  
Author(s):  
Tiago F. Leao ◽  
Chase M. Clark ◽  
Anelize Bauermeister ◽  
Emmanuel O. Elijah ◽  
Emily C. Gentry ◽  
...  
Keyword(s):  
Untargeted Metabolomics ◽  
Metabolomics Analysis

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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