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Book ; Thesis: Characterization of the two PPAR target genes FIAF (fasting-induced adipose factor) and G0S2 (G0/G1 switch gene 2)

Zandbergen, Fokko J

2006

Author's details	Fokko J. Zandbergen
Language	English
Size	136 p. :, ill. ;, 24 cm.
Publisher	s.n
Publishing place	Wageningen
Document type	Book ; Thesis
Thesis / German Habilitation thesis	Thesis (doctoral)--Wageningen Universiteit, 2006
Note	Summary in Dutch. ; Vita. ; "Stellingen" inserted.
ISBN	9085043921 ; 9789085043928
Database	NAL-Catalogue (AGRICOLA)

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Article: PPARalpha in atherosclerosis and inflammation.

Zandbergen, Fokko / Plutzky, Jorge

Biochimica et biophysica acta

2007 Volume 1771, Issue 8, Page(s) 972–982

Abstract: Peroxisome proliferator-activated receptor (PPAR)alpha is a nuclear receptor activated by natural ligands such as fatty acids as well as by synthetic ligands such as fibrates currently used to treat dyslipidemia. PPARalpha regulates the expression of ... ...

Abstract	Peroxisome proliferator-activated receptor (PPAR)alpha is a nuclear receptor activated by natural ligands such as fatty acids as well as by synthetic ligands such as fibrates currently used to treat dyslipidemia. PPARalpha regulates the expression of genes encoding proteins that are involved in lipid metabolism, fatty acid oxidation, and glucose homeostasis, thereby improving markers for atherosclerosis and insulin resistance. In addition, PPARalpha exerts anti-inflammatory effects both in the vascular wall and the liver. Here we provide an overview of the mechanisms through which PPARalpha affects the initiation and progression of atherosclerosis, with emphasis on the modulation of atherosclerosis-associated inflammatory responses. PPARalpha activation interferes with early steps in atherosclerosis by reducing leukocyte adhesion to activated endothelial cells of the arterial vessel wall and inhibiting subsequent transendothelial leukocyte migration. In later stages of atherosclerosis, evidence suggests activation of PPARalpha inhibits the formation of macrophage foam cells by regulating expression of genes involved in reverse cholesterol transport, formation of reactive oxygen species (ROS), and associated lipoprotein oxidative modification among others. Furthermore, PPARalpha may increase the stability of atherosclerotic plaques and limit plaque thrombogenicity. These various effects may be linked to the generation of PPARalpha ligands by endogenous mechanisms of lipoprotein metabolism. In spite of this dataset, other reports implicate PPARalpha in responses such as hypertension and diabetic cardiomyopathy. Although some clinical trials data with fibrates suggest that fibrates may decrease cardiovascular events, other studies have been less clear, in terms of benefit. Independent of the clinical effects of currently used drugs purported to achieve PPARalpha, extensive data establish the importance of PPARalpha in the transcriptional regulation of lipid metabolism, atherosclerosis, and inflammation.
MeSH term(s)	Atherosclerosis/immunology ; Atherosclerosis/physiopathology ; Cell Adhesion ; Cytokines/physiology ; Endothelium, Vascular/physiopathology ; Humans ; Inflammation/immunology ; Inflammation/physiopathology ; Leukocytes/physiology ; Liver/physiopathology ; PPAR alpha/immunology ; PPAR alpha/physiology
Chemical Substances	Cytokines ; PPAR alpha
Language	English
Publishing date	2007-08
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	60-7
ISSN	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbalip.2007.04.021
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Article ; Online: Chronic exposure to low-dose arsenic modulates lipogenic gene expression in mice.

Adebayo, Adeola O / Zandbergen, Fokko / Kozul-Horvath, Courtney D / Gruppuso, Philip A / Hamilton, Joshua W

Journal of biochemical and molecular toxicology

2014 Volume 29, Issue 1, Page(s) 1–9

Abstract: Arsenic, a ubiquitous environmental toxicant, can affect lipid metabolism through mechanisms that are not well understood. We studied the effect of arsenic on serum lipids, lipid-regulating genes, and transcriptional regulator sterol regulatory element ... ...

Abstract	Arsenic, a ubiquitous environmental toxicant, can affect lipid metabolism through mechanisms that are not well understood. We studied the effect of arsenic on serum lipids, lipid-regulating genes, and transcriptional regulator sterol regulatory element binding protein 1c (SREBP-1c). C57BL/6 mice were administered 0 or 100 ppb sodium arsenite in drinking water for 5 weeks. Arsenic exposure was associated with decreased liver weight but no change in body weight. Serum triglycerides level fell in arsenic-exposed animals, but not in fed animals, after short-term fasting. Hepatic expression of SREBP-1c was reduced in arsenic-exposed fed animals, with a 16-fold change in reduction. Similar effects were seen for SREBP-1c in white adipose tissue. However, fasting resulted in dissociation of the expression of SREBP-1c and its targets, and SREBP-1c protein content could not be shown to correlate with its mRNA expression. We conclude that arsenic modulates hepatic expression of genes involved in lipid regulation through mechanisms that are independent of SREBP-1c expression.
MeSH term(s)	Adipose Tissue, White/metabolism ; Animals ; Arsenic/pharmacology ; Arsenites/pharmacology ; Enzyme Inhibitors/pharmacology ; Gene Expression Regulation/drug effects ; Lipogenesis/drug effects ; Liver/metabolism ; Male ; Mice ; Sodium Compounds/pharmacology ; Sterol Regulatory Element Binding Protein 1/biosynthesis ; Triglycerides/biosynthesis
Chemical Substances	Arsenites ; Enzyme Inhibitors ; Sodium Compounds ; Srebf1 protein, mouse ; Sterol Regulatory Element Binding Protein 1 ; Triglycerides ; sodium arsenite (48OVY2OC72) ; Arsenic (N712M78A8G)
Language	English
Publishing date	2014-08-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1410020-4
ISSN	1099-0461 ; 1095-6670
ISSN (online)	1099-0461
ISSN	1095-6670
DOI	10.1002/jbt.21600
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Article ; Online: Effects of low-dose drinking water arsenic on mouse fetal and postnatal growth and development.

Kozul-Horvath, Courtney D / Zandbergen, Fokko / Jackson, Brian P / Enelow, Richard I / Hamilton, Joshua W

PloS one

2012 Volume 7, Issue 5, Page(s) e38249

Abstract: Background: Arsenic (As) exposure is a significant worldwide environmental health concern. Chronic exposure via contaminated drinking water has been associated with an increased incidence of a number of diseases, including reproductive and developmental ...

Abstract	Background: Arsenic (As) exposure is a significant worldwide environmental health concern. Chronic exposure via contaminated drinking water has been associated with an increased incidence of a number of diseases, including reproductive and developmental effects. The goal of this study was to identify adverse outcomes in a mouse model of early life exposure to low-dose drinking water As (10 ppb, current U.S. EPA Maximum Contaminant Level). Methodology and findings: C57B6/J pups were exposed to 10 ppb As, via the dam in her drinking water, either in utero and/or during the postnatal period. Birth outcomes, the growth of the F1 offspring, and health of the dams were assessed by a variety of measurements. Birth outcomes including litter weight, number of pups, and gestational length were unaffected. However, exposure during the in utero and postnatal period resulted in significant growth deficits in the offspring after birth, which was principally a result of decreased nutrients in the dam's breast milk. Cross-fostering of the pups reversed the growth deficit. Arsenic exposed dams displayed altered liver and breast milk triglyceride levels and serum profiles during pregnancy and lactation. The growth deficits in the F1 offspring resolved following separation from the dam and cessation of exposure in male mice, but did not resolve in female mice up to six weeks of age. Conclusions/significance: Exposure to As at the current U.S. drinking water standard during critical windows of development induces a number of adverse health outcomes for both the dam and offspring. Such effects may contribute to the increased disease risks observed in human populations.
MeSH term(s)	Animal Husbandry ; Animals ; Arsenic/metabolism ; Arsenic/pharmacology ; Dose-Response Relationship, Drug ; Drinking Water/chemistry ; Female ; Fetus/drug effects ; Growth and Development/drug effects ; Lactation/drug effects ; Male ; Mice ; Mice, Inbred C57BL ; Milk, Human/drug effects ; Milk, Human/metabolism ; Pregnancy ; Triglycerides/metabolism ; Water Pollutants, Chemical/pharmacology
Chemical Substances	Drinking Water ; Triglycerides ; Water Pollutants, Chemical ; Arsenic (N712M78A8G)
Language	English
Publishing date	2012-05-31
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0038249
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Use of Nano Seed Crystals To Control Peroxide Morphology in a Nonaqueous Li–O2 Battery

Ganapathy, Swapna / Li Zhaolong / Anastasaki Maria S / Basak Shibabrata / Miao Xue-Fei / Goubitz Kees / Zandbergen HennyW / Mulder Fokko M / Wagemaker Marnix

The Journal of Physical Chemistry C. 2016 Aug. 25, v. 120, no. 33

2016

Abstract: The high theoretical energy density of Li–O₂ batteries as required for electrification of transport has pushed Li–O₂ research to the forefront. The poor cyclability of this system due to incomplete Li₂O₂ oxidation is one of the major hurdles to be ... ...

Abstract	The high theoretical energy density of Li–O₂ batteries as required for electrification of transport has pushed Li–O₂ research to the forefront. The poor cyclability of this system due to incomplete Li₂O₂ oxidation is one of the major hurdles to be crossed if it is ever to deliver a high reversible energy density. Here we present the use of nano seed crystallites to control the size and morphology of the Li₂O₂ crystals. The evolution of the Li₂O₂ lattice parameters during operando X-ray diffraction demonstrates that the hexagonal NiO nanoparticles added to the activated carbon electrode act as seed crystals for equiaxed growth of Li₂O₂, which is confirmed by scanning electron microscopy energy-dispersive X-ray spectroscopy (SEM-EDX) elemental maps also showing preferential formation of Li₂O₂ on the NiO surface. Even small amounts of NiO (∼5 wt %) particles act as preferential sites for Li₂O₂ nucleation, effectively reducing the average size of the primary Li₂O₂ crystallites and promoting crystalline growth. This is supported by first principle calculations, which predict a low interfacial energy for the formation of NiO–Li₂O₂ interfaces. The eventual cell failure appears to be the consequence of electrolyte side reactions, indicating the necessity of more stable electrolytes. The demonstrated control of the Li₂O₂ crystallite growth by the rational selection of appropriate nano seed crystals appears to be a promising strategy to improve the reversibility of Li–air electrodes.
Keywords	X-ray diffraction ; activated carbon ; batteries ; carbon electrodes ; crystallites ; electrolytes ; energy ; energy density ; energy-dispersive X-ray analysis ; nanoparticles ; nickel oxide ; oxidation ; physical chemistry ; scanning electron microscopy
Language	English
Dates of publication	2016-0825
Size	p. 18421-18427.
Publishing place	American Chemical Society
Document type	Article
ISSN	1932-7455
DOI	10.1021%2Facs.jpcc.6b04732
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Article ; Online: Effects of low-dose drinking water arsenic on mouse fetal and postnatal growth and development.

Courtney D Kozul-Horvath / Fokko Zandbergen / Brian P Jackson / Richard I Enelow / Joshua W Hamilton

PLoS ONE, Vol 7, Iss 5, p e

2012 Volume 38249

Abstract: Arsenic (As) exposure is a significant worldwide environmental health concern. Chronic exposure via contaminated drinking water has been associated with an increased incidence of a number of diseases, including reproductive and developmental effects. The ...

Abstract	Arsenic (As) exposure is a significant worldwide environmental health concern. Chronic exposure via contaminated drinking water has been associated with an increased incidence of a number of diseases, including reproductive and developmental effects. The goal of this study was to identify adverse outcomes in a mouse model of early life exposure to low-dose drinking water As (10 ppb, current U.S. EPA Maximum Contaminant Level).C57B6/J pups were exposed to 10 ppb As, via the dam in her drinking water, either in utero and/or during the postnatal period. Birth outcomes, the growth of the F1 offspring, and health of the dams were assessed by a variety of measurements. Birth outcomes including litter weight, number of pups, and gestational length were unaffected. However, exposure during the in utero and postnatal period resulted in significant growth deficits in the offspring after birth, which was principally a result of decreased nutrients in the dam's breast milk. Cross-fostering of the pups reversed the growth deficit. Arsenic exposed dams displayed altered liver and breast milk triglyceride levels and serum profiles during pregnancy and lactation. The growth deficits in the F1 offspring resolved following separation from the dam and cessation of exposure in male mice, but did not resolve in female mice up to six weeks of age.Exposure to As at the current U.S. drinking water standard during critical windows of development induces a number of adverse health outcomes for both the dam and offspring. Such effects may contribute to the increased disease risks observed in human populations.
Keywords	Medicine ; R ; Science ; Q
Subject code	333
Language	English
Publishing date	2012-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
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Article: Identification of VP19 and VP15 of white spot syndrome virus (WSSV) and glycosylation status of the WSSV major structural proteins.

van Hulten, Mariëlle C W / Reijns, Martin / Vermeesch, Angela M G / Zandbergen, Fokko / Vlak, Just M

The Journal of general virology

2002 Volume 83, Issue Pt 1, Page(s) 257–265

Abstract: White spot syndrome virus (WSSV) infects penaeid shrimp and other crustaceans. The WSSV virion consists of an enveloped rod-shaped nucleocapsid enclosing a large circular double-stranded DNA genome of 293 kbp. The virion envelope contains two major ... ...

Abstract	White spot syndrome virus (WSSV) infects penaeid shrimp and other crustaceans. The WSSV virion consists of an enveloped rod-shaped nucleocapsid enclosing a large circular double-stranded DNA genome of 293 kbp. The virion envelope contains two major proteins of 28 (VP28) and 19 kDa (VP19) and the nucleocapsid consists of three major proteins of 26 (VP26), 24 (VP24) and 15 kDa (VP15). Study on the morphogenesis of the WSSV particle requires the genomic identification and chemical characterization of these WSSV virion proteins. An internal amino acid sequence of envelope protein VP19 was obtained by amino acid sequencing and used to locate the VP19 open reading frame of this protein on the genome, as WSSV ORF182. VP19 contained two putative transmembrane domains, which may anchor this protein in the WSSV envelope. Similarly, the gene for VP15 was located on the WSSV genome as ORF109. N-terminal amino acid sequencing on VP15 suggested that this protein was expressed from the second ATG of its ORF and the first methionine is lost by N-terminal protein processing. The 15 kDa protein is very basic and is a candidate DNA-binding protein in the WSSV nucleocapsid. None of the five major structural WSSV proteins appear to be glycosylated, which is an unusual feature among enveloped animal viruses.
MeSH term(s)	Amino Acid Sequence ; Animals ; Astacoidea ; Base Sequence ; Cell Line ; DNA Viruses/genetics ; DNA Viruses/metabolism ; DNA, Viral ; Decapoda/virology ; Genes, Viral ; Genome, Viral ; Glycosylation ; Molecular Sequence Data ; Nucleocapsid Proteins/genetics ; Nucleocapsid Proteins/metabolism ; Viral Envelope Proteins/genetics ; Viral Envelope Proteins/metabolism ; Virion
Chemical Substances	DNA, Viral ; Nucleocapsid Proteins ; VP15 protein, white spot syndrome virus ; VP19 protein, white spot syndrome virus ; Viral Envelope Proteins
Language	English
Publishing date	2002-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	219316-4
ISSN	1465-2099 ; 0022-1317
ISSN (online)	1465-2099
ISSN	0022-1317
DOI	10.1099/0022-1317-83-1-257
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Article: The fasting-induced adipose factor/angiopoietin-like protein 4 is physically associated with lipoproteins and governs plasma lipid levels and adiposity.

Mandard, Stéphane / Zandbergen, Fokko / van Straten, Esther / Wahli, Walter / Kuipers, Folkert / Müller, Michael / Kersten, Sander

The Journal of biological chemistry

2005 Volume 281, Issue 2, Page(s) 934–944

Abstract: Proteins secreted from adipose tissue are increasingly recognized to play an important role in the regulation of glucose metabolism. However, much less is known about their effect on lipid metabolism. The fasting-induced adipose factor (FIAF/angiopoietin- ...

Abstract	Proteins secreted from adipose tissue are increasingly recognized to play an important role in the regulation of glucose metabolism. However, much less is known about their effect on lipid metabolism. The fasting-induced adipose factor (FIAF/angiopoietin-like protein 4/peroxisome proliferator-activated receptor gamma angiopoietin-related protein) was previously identified as a target of hypolipidemic fibrate drugs and insulin-sensitizing thiazolidinediones. Using transgenic mice that mildly overexpress FIAF in peripheral tissues we show that FIAF is an extremely powerful regulator of lipid metabolism and adiposity. FIAF overexpression caused a 50% reduction in adipose tissue weight, partly by stimulating fatty acid oxidation and uncoupling in fat. In addition, FIAF overexpression increased plasma levels of triglycerides, free fatty acids, glycerol, total cholesterol, and high density lipoprotein (HDL)-cholesterol. Functional tests indicated that FIAF overexpression severely impaired plasma triglyceride clearance but had no effect on very low density lipoprotein production. The effects of FIAF overexpression were amplified by a high fat diet, resulting in markedly elevated plasma and liver triglycerides, plasma free fatty acids, and plasma glycerol levels, and impaired glucose tolerance in FIAF transgenic mice fed a high fat diet. Remarkably, in mice the full-length form of FIAF was physically associated with HDL, whereas truncated FIAF was associated with low density lipoprotein. In human both full-length and truncated FIAF were associated with HDL. The composite data suggest that via physical association with plasma lipoproteins, FIAF acts as a powerful signal from fat and other tissues to prevent fat storage and stimulate fat mobilization. Our data indicate that disturbances in FIAF signaling might be involved in dyslipidemia.
MeSH term(s)	Adipose Tissue/metabolism ; Angiopoietin-like 4 Protein ; Angiopoietins ; Animals ; Blood Proteins/chemistry ; Blood Proteins/genetics ; Blood Proteins/physiology ; Body Weight ; Cholesterol/metabolism ; Fats/chemistry ; Gene Expression ; Glucose/metabolism ; Glucose Tolerance Test ; Humans ; Hypercholesterolemia/metabolism ; Immunoblotting ; Insulin/metabolism ; Lipase/metabolism ; Lipids/chemistry ; Lipoproteins/chemistry ; Lipoproteins, HDL/chemistry ; Lipoproteins, HDL/metabolism ; Lipoproteins, LDL/chemistry ; Lipoproteins, VLDL/chemistry ; Liver/enzymology ; Male ; Mice ; Mice, Transgenic ; Models, Genetic ; Oligonucleotide Array Sequence Analysis ; Protein Binding ; RNA, Messenger/metabolism ; Signal Transduction ; Time Factors ; Triglycerides/blood ; Triglycerides/metabolism ; Up-Regulation
Chemical Substances	Angiopoietin-like 4 Protein ; Angiopoietins ; Angptl4 protein, mouse ; Blood Proteins ; Fats ; Insulin ; Lipids ; Lipoproteins ; Lipoproteins, HDL ; Lipoproteins, LDL ; Lipoproteins, VLDL ; RNA, Messenger ; Triglycerides ; Cholesterol (97C5T2UQ7J) ; Lipase (EC 3.1.1.3) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2005-11-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.M506519200
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Article ; Online: The G0/G1 switch gene 2 is a novel PPAR target gene.

Zandbergen, Fokko / Mandard, Stéphane / Escher, Pascal / Tan, Nguan Soon / Patsouris, David / Jatkoe, Tim / Rojas-Caro, Sandra / Madore, Steve / Wahli, Walter / Tafuri, Sherrie / Müller, Michael / Kersten, Sander

The Biochemical journal

2005 Volume 392, Issue Pt 2, Page(s) 313–324

Abstract: PPARs (peroxisome-proliferator-activated receptors) alpha, beta/delta and gamma are a group of transcription factors that are involved in numerous processes, including lipid metabolism and adipogenesis. By comparing liver mRNAs of wild-type and PPARalpha- ...

Abstract	PPARs (peroxisome-proliferator-activated receptors) alpha, beta/delta and gamma are a group of transcription factors that are involved in numerous processes, including lipid metabolism and adipogenesis. By comparing liver mRNAs of wild-type and PPARalpha-null mice using microarrays, a novel putative target gene of PPARalpha, G0S2 (G0/G1 switch gene 2), was identified. Hepatic expression of G0S2 was up-regulated by fasting and by the PPARalpha agonist Wy14643 in a PPARalpha-dependent manner. Surprisingly, the G0S2 mRNA level was highest in brown and white adipose tissue and was greatly up-regulated during mouse 3T3-L1 and human SGBS (Simpson-Golabi-Behmel syndrome) adipogenesis. Transactivation, gel shift and chromatin immunoprecipitation assays indicated that G0S2 is a direct PPARgamma and probable PPARalpha target gene with a functional PPRE (PPAR-responsive element) in its promoter. Up-regulation of G0S2 mRNA seemed to be specific for adipogenesis, and was not observed during osteogenesis or myogenesis. In 3T3-L1 fibroblasts, expression of G0S2 was associated with growth arrest, which is required for 3T3-L1 adipogenesis. Together, these data indicate that G0S2 is a novel target gene of PPARs that may be involved in adipocyte differentiation.
MeSH term(s)	Adipocytes/cytology ; Adipocytes/metabolism ; Adipogenesis ; Animals ; Base Sequence ; Cell Cycle Proteins/genetics ; Cell Cycle Proteins/metabolism ; Cell Line ; Endoplasmic Reticulum/metabolism ; Gene Deletion ; Hepatocytes/cytology ; Hepatocytes/metabolism ; Humans ; Liver/cytology ; Male ; Mice ; Molecular Sequence Data ; Oligonucleotide Array Sequence Analysis ; PPAR alpha/genetics ; PPAR alpha/metabolism ; Promoter Regions, Genetic/genetics ; Protein Transport ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Rats ; Response Elements/genetics ; Sequence Homology, Nucleic Acid ; Substrate Specificity ; Up-Regulation
Chemical Substances	Cell Cycle Proteins ; G0S2 protein, human ; G0S2 protein, mouse ; PPAR alpha ; RNA, Messenger
Language	English
Publishing date	2005-12-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2969-5
ISSN	1470-8728 ; 0006-2936 ; 0306-3275 ; 0264-6021
ISSN (online)	1470-8728
ISSN	0006-2936 ; 0306-3275 ; 0264-6021
DOI	10.1042/BJ20050636
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Article: The direct peroxisome proliferator-activated receptor target fasting-induced adipose factor (FIAF/PGAR/ANGPTL4) is present in blood plasma as a truncated protein that is increased by fenofibrate treatment.

Mandard, Stéphane / Zandbergen, Fokko / Tan, Nguan Soon / Escher, Pascal / Patsouris, David / Koenig, Wolfgang / Kleemann, Robert / Bakker, Arjen / Veenman, Frank / Wahli, Walter / Müller, Michael / Kersten, Sander

The Journal of biological chemistry

2004 Volume 279, Issue 33, Page(s) 34411–34420

Abstract: The fasting-induced adipose factor (FIAF, ANGPTL4, PGAR, HFARP) was previously identified as a novel adipocytokine that was up-regulated by fasting, by peroxisome proliferator-activated receptor agonists, and by hypoxia. To further characterize FIAF, we ... ...

Abstract	The fasting-induced adipose factor (FIAF, ANGPTL4, PGAR, HFARP) was previously identified as a novel adipocytokine that was up-regulated by fasting, by peroxisome proliferator-activated receptor agonists, and by hypoxia. To further characterize FIAF, we studied regulation of FIAF mRNA and protein in liver and adipose cell lines as well as in human and mouse plasma. Expression of FIAF mRNA was up-regulated by peroxisome proliferator-activated receptor alpha (PPARalpha) and PPARbeta/delta agonists in rat and human hepatoma cell lines and by PPARgamma and PPARbeta/delta agonists in mouse and human adipocytes. Transactivation, chromatin immunoprecipitation, and gel shift experiments identified a functional PPAR response element within intron 3 of the FIAF gene. At the protein level, in human and mouse blood plasma, FIAF was found to be present both as the native protein and in a truncated form. Differentiation of mouse 3T3-L1 adipocytes was associated with the production of truncated FIAF, whereas in human white adipose tissue and SGBS adipocytes, only native FIAF could be detected. Interestingly, truncated FIAF was produced by human liver. Treatment with fenofibrate, a potent PPARalpha agonist, markedly increased plasma levels of truncated FIAF, but not native FIAF, in humans. Levels of both truncated and native FIAF showed marked interindividual variation but were not associated with body mass index and were not influenced by prolonged semistarvation. Together, these data suggest that FIAF, similar to other adipocytokines such as adiponectin, may partially exert its function via a truncated form.
MeSH term(s)	3T3-L1 Cells ; Adipocytes/metabolism ; Adipokines/metabolism ; Adiponectin ; Adipose Tissue/metabolism ; Angiopoietin-like 4 Protein ; Angiopoietins ; Animals ; Base Sequence ; Blotting, Western ; Cell Differentiation ; Cell Line ; Cell Line, Tumor ; Cells, Cultured ; Chromatin/metabolism ; Cytokines/metabolism ; Fenofibrate/metabolism ; Fenofibrate/pharmacology ; Humans ; Intercellular Signaling Peptides and Proteins/blood ; Introns ; Liver/metabolism ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Precipitin Tests ; Proteins/metabolism ; RNA/metabolism ; RNA, Messenger/metabolism ; Rats ; Receptors, Cytoplasmic and Nuclear/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Transcription Factors/metabolism ; Transcription, Genetic ; Transcriptional Activation ; Up-Regulation
Chemical Substances	ANGPTL4 protein, human ; ANGPTL4 protein, rat ; Adipokines ; Adiponectin ; Angiopoietin-like 4 Protein ; Angiopoietins ; Chromatin ; Cytokines ; Intercellular Signaling Peptides and Proteins ; Proteins ; RNA, Messenger ; Receptors, Cytoplasmic and Nuclear ; Transcription Factors ; RNA (63231-63-0) ; Fenofibrate (U202363UOS)
Language	English
Publishing date	2004-06-09
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.M403058200
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