PRIC295, a Nuclear Receptor Coactivator, Identified from PPAR-Interacting Cofactor Complex

Pyper, Sean R.; Viswakarma, Navin; Jia, Yuzhi; Zhu, Yijun; Fondell, Joseph D.; Reddy, Janardan K.

doi:10.1155/2010/173907

Cited by 14 publications

(4 citation statements)

References 91 publications

(121 reference statements)

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“…These results suggest the possible involvement of peroxisomal metabolism in obesity. Therefore, the regulation of PPARα activity through modulating endogenous ligands may have the potential to generate a new therapeutic approach for obesity and lifestyle-related diseases (5). In the present study, in order to obtain insight into the role of peroxisomal metabolism, particularly VLCFA metabolism in obesity, we compared the levels of VLCFAs in plasma.…”

Section: Introductionmentioning

confidence: 99%

Induction of peroxisomal lipid metabolism in mice fed a high-fat diet

et al. 2011

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Abstract. Peroxisomes catalyze a range of essential metabolic functions, mainly related to lipid metabolism. However, their roles in obesity have yet to be clarified. The aim of this study was to investigate the correlation between obesity and peroxisomal lipid metabolism, particularly very long-chain fatty acid (VLCFA) metabolism, gene expression of peroxisomal β-oxidation enzymes, peroxisomal ATP-binding cassette (ABC) transporter adrenoleukodystrophy (ABCD1) gene and its related gene, ABCD2, the elongation of the VLCFA (ELOVL) gene family and the transcriptional factors involved in the regulation of these genes, including peroxisome proliferator-activated receptor α (PPARα) and sterol regulatory element-binding protein. These factors were analyzed in livers from mice fed a high-fat diet (HFD) or a regular diet (RD) for 20 weeks. Furthermore, the amounts of plasma saturated and unsaturated fatty acids, including VLCFAs, were measured. A HFD induced hepatic gene expression of not only hydroxysteroid 17-β dehydrogenase 4 (HSD17b4) and sterol carrier protein 2 (SCP2) in peroxisomal β-oxidation enzymes but also of ELOVL1, 2, 5 and 6, which are involved in the elongation of saturated and unsaturated VLCFAs. Furthermore, ABCD2 mRNA prominently increased in the HFD mice. The transcriptional regulator of these genes, PPARα, was also up-regulated in the HFD mice. VLCFA ratios including C24:0/ C22:0, C25:0/C22:0 and C26:0/C22:0 are the most significant diagnostic markers of inherited peroxisomal diseases. These ratios were found to be low in the plasma of the HFD mice compared with the RD mice. The results suggest that HFD activates hepatic peroxisomal VLCFA metabolism, and may provide useful fundamental information to explain the role of peroxisomal function in obesity and lifestyle-related diseases.

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Section: Introductionmentioning

confidence: 99%

Induction of peroxisomal lipid metabolism in mice fed a high-fat diet

et al. 2011

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“…In rats, these compounds have been also associated with hepatocellular adenomas ( Lau et al 2007 ). In mice, one of the biological effects of PFAAs is the activation of the peroxisome proliferator-activated receptor-α (PPAR-α), a ligand--activated transcription factor that regulates gene expression, lipid modulation, glucose homeostasis, cell proliferation, and inflammation ( Pyper et al 2010 ). Although some effects in experimental studies are mediated by PPAR-α binding, some other effects occur independently of this receptor ( Bjork et al 2011 ; Ren et al 2009 ).…”

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confidence: 99%

Serum Perfluorooctanoate (PFOA) and Perfluorooctane Sulfonate (PFOS) Concentrations and Liver Function Biomarkers in a Population with Elevated PFOA Exposure

Gallo

Leonardi

Genser

et al. 2012

Environ Health Perspect

225

138

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Background: Perfluorooctanoate (PFOA) and perfluorooctane sulfonate (PFOS) persist in the environment and are found in relatively high concentrations in animal livers. Studies in humans have reported inconsistent associations between PFOA and liver enzymes.Objectives: We examined the cross-sectional association between serum PFOA and PFOS concentrations with markers of liver function in adults.Methods: The C8 Health Project collected data on 69,030 persons; of these, a total of 47,092 adults were included in the present analysis. Linear regression models were fitted for natural log (ln)-transformed values of alanine transaminase (ALT), γ-glutamyltransferase (GGT), and direct bilirubin on PFOA, PFOS, and potential confounders. Logistic regression models were fitted comparing deciles of PFOA or PFOS in relation to high biomarker levels. A multilevel analysis comparing the evidence for association of PFOA with liver function at the individual level within water districts to that at the population level between water districts was also performed.Results: ln-PFOA and ln-PFOS were associated with ln-ALT in linear regression models [PFOA: coefficient, 0.022; 95% confidence interval (CI): 0.018, 0.025; PFOS: coefficient, 0.020; 95% CI: 0.014, 0.026] and with raised ALT in logistic regression models [with a steady increase in the odds ratio (OR) estimates across deciles of PFOA and PFOS; PFOA: OR = 1.10; 95% CI: 1.07, 1.13; PFOS: OR = 1.13; 95% CI: 1.07, 1.18]. There was less consistent evidence of an association of PFOA and GGT or bilirubin. The relationship with bilirubin appears to rise at low levels of PFOA and to fall again at higher levels.Conclusions: These results show a positive association between PFOA and PFOS concentrations and serum ALT level, a marker of hepatocellular damage.

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“…e effect of PFOA and PFOS on PPARα also occurs via the COS-1 human cell line transiently transfected with a luciferase reporter gene [188]. Because PPARs are transcription factors responsible for controlling lipid modulation, gene expression, glucose homeostasis, cell proliferation, and inflammation processes, their activation contributes to the proliferation of peroxisomes and the catabolism of fatty acids and cholesterol [189]. Proliferation of peroxisomes is one of the main reasons for liver toxicity observed in laboratory animal studies.…”

Section: Toxicological Studies Of Pfaasmentioning

confidence: 99%

A Review of Perfluoroalkyl Acids (PFAAs) in terms of Sources, Applications, Human Exposure, Dietary Intake, Toxicity, Legal Regulation, and Methods of Determination

Sznajder‐Katarzyńska

Surma

Cieślik

2019

Journal of Chemistry

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Per- and polyfluoroalkyl substances (PFASs) are widely distributed across the world and are expected to be of concern to human health and the environment. The review focuses on perfluoroalkyl acids (PFAAs) and, in particular, on the most frequently discussed perfluoroalkyl carboxylic acids (PFCAs) and perfluoroalkane sulfonic acids (PFSAs). In this study, some basic information concerning PFASs is reviewed, focusing mainly on PFAAs (perfluoroalkyl acids). We have made efforts to systemize their division into groups according to chemical structure, describe their basic physicochemical properties, characterize production technologies, and determine potential human exposure routes with particular reference to oral exposure. A variety of possible toxicological effects to human health are also discussed. In response to increasing public concern about the toxicity of PFAAs, an evaluation of dietary intake has been undertaken for two of the most commonly known PFAAs: perfluorooctanoic acid (PFOA) and perfluorooctane sulfonic acid (PFOS). As summarized in this study, PFAAs levels need further assessment due to the science-based TWI standards laid down by the EFSA’s CONTAM Panel regarding the risk to human health posed by the presence of perfluorooctane sulfonic acid and perfluorooctanoic acid in food (tolerable weekly intakes of PFOA and PFOS set up to 6 ng·kg−1·bw·week−1 and 13 ng·kg−1·bw·week−1, respectively). Current legislation, relevant legislation on PFAAs levels in food, and the most popular methods of analysis in food matrices are described.

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PRIC295, a Nuclear Receptor Coactivator, Identified from PPAR-Interacting Cofactor Complex

Cited by 14 publications

References 91 publications

Induction of peroxisomal lipid metabolism in mice fed a high-fat diet

Induction of peroxisomal lipid metabolism in mice fed a high-fat diet

Serum Perfluorooctanoate (PFOA) and Perfluorooctane Sulfonate (PFOS) Concentrations and Liver Function Biomarkers in a Population with Elevated PFOA Exposure

A Review of Perfluoroalkyl Acids (PFAAs) in terms of Sources, Applications, Human Exposure, Dietary Intake, Toxicity, Legal Regulation, and Methods of Determination

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