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Article ; Online: Interaction between fatty acid oxidation and ethanol metabolism in liver.

Lu, Yongke / George, Joseph

American journal of physiology. Gastrointestinal and liver physiology

2024 Volume 326, Issue 5, Page(s) G483–G494

Abstract: Fatty acid oxidation (FAO) releases the energy stored in fat to maintain basic biological processes. Dehydrogenation is a major way to oxidize fatty acids, which needs ... ...

Abstract	Fatty acid oxidation (FAO) releases the energy stored in fat to maintain basic biological processes. Dehydrogenation is a major way to oxidize fatty acids, which needs NAD
MeSH term(s)	Humans ; Catalase ; NAD ; Cytochrome P-450 CYP2E1 ; Hydrogen Peroxide ; Fatty Liver ; Ethanol ; Liver Diseases, Alcoholic ; Fatty Acids
Chemical Substances	Catalase (EC 1.11.1.6) ; NAD (0U46U6E8UK) ; Cytochrome P-450 CYP2E1 (EC 1.14.13.-) ; Hydrogen Peroxide (BBX060AN9V) ; Ethanol (3K9958V90M) ; Fatty Acids
Language	English
Publishing date	2024-03-05
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	603840-2
ISSN	1522-1547 ; 0193-1857
ISSN (online)	1522-1547
ISSN	0193-1857
DOI	10.1152/ajpgi.00281.2023
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Article ; Online: Alcoholic fatty liver is blunted by rFGF21 administration in mice lacking adipose FGFR1: The role of FGF21 in PPARα-mediated regulation of adipose tissue mass.

Xu, Yunhui / Lu, Yongke

Biochemical and biophysical research communications

2022 Volume 619, Page(s) 84–89

Abstract: Fibroblast growth factor 21 (FGF21) is regulated by peroxisome proliferator activated receptor α (PPARα) in the liver. FGF21 regulates lipid metabolism via fibroblast growth factor receptor 1 (FGFR1). FGF21 protect against alcoholic fatty liver (AFL), ... ...

Abstract	Fibroblast growth factor 21 (FGF21) is regulated by peroxisome proliferator activated receptor α (PPARα) in the liver. FGF21 regulates lipid metabolism via fibroblast growth factor receptor 1 (FGFR1). FGF21 protect against alcoholic fatty liver (AFL), however, FGF21 does not exert protective effect through liver FGFR1. We have previously shown that PPARα agonist WY-14,643 induces FGF21 and adipose atrophy but fails to protect against chronic ethanol-induced AFL in mice lacking adipose FGFR1. In this study we tested the direct role of the FGF21 in regulation of adipose tissue mass and ethanol induced-hepatic triglyceride (TG) accumulation in normal control (fgfr1
MeSH term(s)	Adipose Tissue/metabolism ; Animals ; Atrophy ; Ethanol/pharmacology ; Fatty Liver, Alcoholic/metabolism ; Fibroblast Growth Factors/metabolism ; Liver/metabolism ; Mice ; Mice, Knockout ; PPAR alpha/metabolism ; Receptor, Fibroblast Growth Factor, Type 1/genetics ; Receptor, Fibroblast Growth Factor, Type 1/metabolism
Chemical Substances	PPAR alpha ; fibroblast growth factor 21 ; Ethanol (3K9958V90M) ; Fibroblast Growth Factors (62031-54-3) ; Receptor, Fibroblast Growth Factor, Type 1 (EC 2.7.10.1)
Language	English
Publishing date	2022-06-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2022.05.099
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Article: Alcoholic fatty liver is blunted by rFGF21 administration in mice lacking adipose FGFR1: The role of FGF21 in PPARα-mediated regulation of adipose tissue mass

Xu, Yunhui / Lu, Yongke

Biochemical and biophysical research communications. 2022 Sept. 03, v. 619

2022

Abstract	Fibroblast growth factor 21 (FGF21) is regulated by peroxisome proliferator activated receptor α (PPARα) in the liver. FGF21 regulates lipid metabolism via fibroblast growth factor receptor 1 (FGFR1). FGF21 protect against alcoholic fatty liver (AFL), however, FGF21 does not exert protective effect through liver FGFR1. We have previously shown that PPARα agonist WY-14,643 induces FGF21 and adipose atrophy but fails to protect against chronic ethanol-induced AFL in mice lacking adipose FGFR1. In this study we tested the direct role of the FGF21 in regulation of adipose tissue mass and ethanol induced-hepatic triglyceride (TG) accumulation in normal control (fgfr1ᶠˡ/ᶠˡ) mice and in adipose FGFR1 knockout mice (fgfr1ᵃᵈⁱᵖᵒQ⁻ᶜʳᵉ). First, we tested whether WY-14,643 effects on adipose atrophy and AFL can be recapitulated in binge alcohol model. As in chronic model, adipose tissue mass and serum free fatty acid (FFA) were decreased by WY-14,643 in the fgfr1ᵃᵈⁱᵖᵒQ⁻ᶜʳᵉ mice but not in the fgfr1ᶠˡ/ᶠˡ mice. However, in contrast to the chronic model, binge ethanol-induced AFL was blunted by WY-14,643 to a greater extent in the fgfr1ᵃᵈⁱᵖᵒQ⁻ᶜʳᵉ mice than in the fgfr1ᶠˡ/ᶠˡ mice. Similarly, circulating FGF21 was elevated by binge ethanol to a greater extent in the fgfr1ᵃᵈⁱᵖᵒQ⁻ᶜʳᵉ mice than in the fgfr1ᶠˡ/ᶠˡ mice on top of WY-14,643 treatment. Accordingly, we tested the involvement of the FGF21 in adipose atrophy and AFL. Consistent with FGFR1-dependent effects of WY-14,643 on adipose atrophy and AFL, recombinant mouse FGF21 (rFGF21) injection induced adipose atrophy, blunted AFL and serum TG elevation to a greater extent in the fgfr1ᵃᵈⁱᵖᵒQ⁻ᶜʳᵉ mice than in the fgfr1ᶠˡ/ᶠˡ mice. These results indicated the consistency of adipose FGFR1 dependent effect of WY-14,643 and FGF21 in PPARα-mediated regulation of adipose tissue mass and fat mobilization from adipose tissues to the liver, suggesting that adipose tissues crosstalk with liver through an interaction between liver PPARα-FGF21 and adipose FGFR1 to maintain adipose tissue mass.
Keywords	adipose tissue ; agonists ; atrophy ; blood serum ; ethanol ; fatty liver ; fibroblast growth factor receptor 1 ; fibroblast growth factors ; free fatty acids ; lipid metabolism ; liver ; mice ; models ; protective effect ; research ; triacylglycerols
Language	English
Dates of publication	2022-0903
Size	p. 84-89.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	205723-2
ISSN	0006-291X ; 0006-291X
ISSN (online)	0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2022.05.099
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Article ; Online: PPARα agonist WY-14,643 induces the PLA2/COX-2/ACOX1 pathway to enhance peroxisomal lipid metabolism and ameliorate alcoholic fatty liver in mice.

Xu, Yunhui / Denning, Krista L / Lu, Yongke

Biochemical and biophysical research communications

2022 Volume 613, Page(s) 47–52

Abstract: Peroxisome proliferator-activated receptor α (PPARα) regulates fatty acid oxidation (FAO). Usually, very-long chain fatty acids are first activated by acyl-CoA synthetase (ACS) to generate acyl-CoA for oxidation by acyl-CoA oxidase (ACOX) in peroxisomes, ...

Abstract	Peroxisome proliferator-activated receptor α (PPARα) regulates fatty acid oxidation (FAO). Usually, very-long chain fatty acids are first activated by acyl-CoA synthetase (ACS) to generate acyl-CoA for oxidation by acyl-CoA oxidase (ACOX) in peroxisomes, and the resultant shorter chain fatty acids will be further oxidized in mitochondria. ACS long-chain family member 4 (ACSL4) preferentially uses arachidonic acid (AA) as substrates to synthesize arachidonoyl-CoA. Arachidonoyl-CoA is usually esterified into phospholipids. When AA is released by phospholipase A2 (PLA2) from phospholipids, it will be used for prostaglandin synthesis by cyclooxygenases (COX). In this study, when PPARα agonist WY-14,643 was mixed in liquid Lieber-DeCarli ethanol or control diets and fed to mice, liver PLA2, COX-2, and ACOX1 were induced but ACSL4 was inhibited, suggesting that AA released by PLA2 from phospholipid will be metabolized to prostaglandin via COX-2 instead of being synthesized into acyl-CoA by ACSL4. However, liver prostaglandin E2 (PGE2), a major component of prostaglandin, was not increased with the induced COX-2 but decreased by WY-14,643. ACOX1 specific inhibitor mixed in the liquid diets restored both the WY-14,643-suppressed liver TG and PGE2, but COX-2 specific inhibitor celecoxib mixed in the liquid diets reversed the WY-14,643-suppressed liver TG but not liver PGE2 contents. These results suggest that induction of PLA2, COX-2 and ACOX1 orchestrates to increase oxidation of AA/PGE2, which constitutes one new mechanism by which PPARα induces peroxisomal FAO and inhibits ethanol-induced liver fat accumulation.
MeSH term(s)	Acyl-CoA Oxidase/metabolism ; Animals ; Coenzyme A/metabolism ; Cyclooxygenase 2/metabolism ; Dinoprostone/metabolism ; Fatty Acids/metabolism ; Fatty Liver, Alcoholic/drug therapy ; Fatty Liver, Alcoholic/metabolism ; Lipid Metabolism/drug effects ; Liver/metabolism ; Mice ; PPAR alpha/agonists ; PPAR alpha/metabolism ; Peroxisomes/drug effects ; Peroxisomes/metabolism ; Phospholipases A2/metabolism ; Phospholipids/metabolism ; Pyrimidines/pharmacology ; Signal Transduction/drug effects
Chemical Substances	Fatty Acids ; PPAR alpha ; Phospholipids ; Pyrimidines ; pirinixic acid (86C4MRT55A) ; Ptgs2 protein, mouse (EC 1.14.99.-) ; Cyclooxygenase 2 (EC 1.14.99.1) ; ACOX1 protein, mouse (EC 1.3.3.6) ; Acyl-CoA Oxidase (EC 1.3.3.6) ; Phospholipases A2 (EC 3.1.1.4) ; Dinoprostone (K7Q1JQR04M) ; Coenzyme A (SAA04E81UX)
Language	English
Publishing date	2022-04-30
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2022.04.132
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Article ; Online: fosA11

Lu, Wei / Zhou, Shihan / Ma, Xueli / Xu, Nuo / Liu, Dongxin / Zhang, Keqing / Zheng, Yongke / Wu, Shenghai

Microbiology spectrum

2023 Volume 12, Issue 2, Page(s) e0254223

Abstract: This study investigated resistance genes corresponding to the fosfomycin resistance phenotype in clinical ... ...

Abstract	This study investigated resistance genes corresponding to the fosfomycin resistance phenotype in clinical isolate
MeSH term(s)	Fosfomycin/pharmacology ; Providencia/genetics ; Anti-Bacterial Agents/pharmacology ; Escherichia coli/genetics ; Microbial Sensitivity Tests ; Chromosomes
Chemical Substances	Fosfomycin (2N81MY12TE) ; Anti-Bacterial Agents
Language	English
Publishing date	2023-12-27
Publishing country	United States
Document type	Journal Article
ZDB-ID	2807133-5
ISSN	2165-0497 ; 2165-0497
ISSN (online)	2165-0497
ISSN	2165-0497
DOI	10.1128/spectrum.02542-23
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Article ; Online: Under peroxisome proliferation acyl-CoA oxidase coordinates with catalase to enhance ethanol metabolism.

Chen, Xue / Denning, Krista L / Mazur, Anna / Lawrence, Logan M / Wang, Xiaodong / Lu, Yongke

Free radical biology & medicine

2023 Volume 208, Page(s) 221–228

Abstract: In peroxisomes, acyl-CoA oxidase (ACOX) oxidizes fatty acids and produces ... ...

Abstract	In peroxisomes, acyl-CoA oxidase (ACOX) oxidizes fatty acids and produces H
MeSH term(s)	Animals ; Mice ; Acyl-CoA Oxidase/genetics ; Acyl-CoA Oxidase/metabolism ; Catalase/genetics ; Catalase/metabolism ; Cell Proliferation ; Ethanol/metabolism ; Fatty Liver/metabolism ; Hydrogen Peroxide/metabolism ; Liver/metabolism ; Mice, Knockout ; NF-E2-Related Factor 2/genetics ; NF-E2-Related Factor 2/metabolism ; Peroxisomes/metabolism ; PPAR alpha/genetics ; PPAR alpha/metabolism
Chemical Substances	Acyl-CoA Oxidase (EC 1.3.3.6) ; Catalase (EC 1.11.1.6) ; Ethanol (3K9958V90M) ; Hydrogen Peroxide (BBX060AN9V) ; NF-E2-Related Factor 2 ; PPAR alpha ; pirinixic acid (86C4MRT55A)
Language	English
Publishing date	2023-08-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	807032-5
ISSN	1873-4596 ; 0891-5849
ISSN (online)	1873-4596
ISSN	0891-5849
DOI	10.1016/j.freeradbiomed.2023.08.016
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Article ; Online: Dynamic Data Augmentation Based on Imitating Real Scene for Lane Line Detection

Qingwang Wang / Lu Wang / Yongke Chi / Tao Shen / Jian Song / Ju Gao / Shiquan Shen

Remote Sensing, Vol 15, Iss 1212, p

2023 Volume 1212

Abstract: With the rapid development of urban ground transportation, lane line detection is gradually becoming a major technological direction to help to realize safe vehicle navigation. However, lane line detection results may have incompleteness issues, such as ... ...

Abstract	With the rapid development of urban ground transportation, lane line detection is gradually becoming a major technological direction to help to realize safe vehicle navigation. However, lane line detection results may have incompleteness issues, such as blurry lane lines and disappearance of the lane lines in the distance, since the lane lines may be heavily obscured by vehicles and pedestrians on the road. In addition, low-visibility environments also pose a challenge for lane line detection. To solve the above problems, we propose a dynamic data augmentation framework based on imitating real scenes (DDA-IRS). DDA-IRS contains three data augmentation strategies that simulate different realistic scenes (i.e., shadows, dazzle, and crowded). In this way, we expand from a limited scene dataset to realistically fit multiple complex scenes. Importantly, DDA-IRS is a lightweight framework that can be integrated with a variety of training-based models without modifying the original model. We evaluate the proposed DDA-IRS on the CULane dataset, and the results show that the data-enhanced model outperforms the baseline model by 0.5% in terms of F-measure. In particular, the F-measure of the “Normal”, “Crowded”, “Shadow”, “Arrow”, and “Curve” achieve a 0.4%, 0.1%, 1.6%, 0.4%, and 1.4% improvement, respectively.
Keywords	dynamic data augmentation ; imitating real scene ; lane line detection ; vehicle navigation ; urban ground transportation ; Science ; Q
Language	English
Publishing date	2023-02-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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Article ; Online: Genome-wide DNA methylation analysis in schizophrenia with tardive dyskinesia: a preliminary study.

Zhang, Ping / Lu, Yongke / Li, Yanli / Wang, Kesheng / An, Huimei / Tan, Yunlong

Genes & genomics

2023 Volume 45, Issue 10, Page(s) 1317–1328

Abstract: Background: Tardive dyskinesia (TD) develops in 20-30% of schizophrenia patients and up to 50% in patients > 50 years old. DNA methylation may play an important role in the development of TD.: Objective: DNA methylation analyses in schizophrenia with ...

Abstract	Background: Tardive dyskinesia (TD) develops in 20-30% of schizophrenia patients and up to 50% in patients > 50 years old. DNA methylation may play an important role in the development of TD. Objective: DNA methylation analyses in schizophrenia with TD. Methods: We conducted a genome-wide DNA methylation analysis in schizophrenia with TD using methylated DNA immunoprecipitation coupled with next-generation sequencing (MeDIP-Seq) in a Chinese sample including five schizophrenia patients with TD and five without TD (NTD), and five healthy controls. The results were expressed as the log Results: Through genome-wide MeDIP-Seq analysis, we identified 116 genes that were significantly differentially methylated in promotor regions in comparison of TD group with NTD group including 66 hypermethylated genes (top 4 genes are GABRR1, VANGL2, ZNF534, and ZNF746) and 50 hypomethylated genes (top 4 genes are DERL3, GSTA4, KNCN, and LRRK1). Part of these genes (such as DERL3, DLGAP2, GABRR1, KLRG2, LRRK1, VANGL2, and ZP3) were previously reported to be associated with methylation in schizophrenia. Gene Ontology enrichment and KEGG pathway analyses identified several pathways. So far, we have confirmed the methylation of 3 genes (ARMC6, WDR75, and ZP3) in schizophrenia with TD using pyrosequencing. Conclusions: This study identified number of methylated genes and pathways for TD and will provide potential biomarkers for TD and serve as a resource for replication in other populations.
MeSH term(s)	Humans ; Middle Aged ; Tardive Dyskinesia/genetics ; DNA Methylation/genetics ; Schizophrenia/genetics ; Genome ; DNA/genetics ; Repressor Proteins/genetics
Chemical Substances	DNA (9007-49-2) ; ZNF746 protein, human ; Repressor Proteins
Language	English
Publishing date	2023-07-06
Publishing country	Korea (South)
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2504587-8
ISSN	2092-9293 ; 1976-9571
ISSN (online)	2092-9293
ISSN	1976-9571
DOI	10.1007/s13258-023-01414-5
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Article: PPARα agonist WY-14,643 induces the PLA2/COX-2/ACOX1 pathway to enhance peroxisomal lipid metabolism and ameliorate alcoholic fatty liver in mice

Xu, Yunhui / Denning, Krista L. / Lu, Yongke

Biochemical and biophysical research communications. 2022 July 12, v. 613

2022

Abstract	Peroxisome proliferator-activated receptor α (PPARα) regulates fatty acid oxidation (FAO). Usually, very-long chain fatty acids are first activated by acyl-CoA synthetase (ACS) to generate acyl-CoA for oxidation by acyl-CoA oxidase (ACOX) in peroxisomes, and the resultant shorter chain fatty acids will be further oxidized in mitochondria. ACS long-chain family member 4 (ACSL4) preferentially uses arachidonic acid (AA) as substrates to synthesize arachidonoyl-CoA. Arachidonoyl-CoA is usually esterified into phospholipids. When AA is released by phospholipase A2 (PLA2) from phospholipids, it will be used for prostaglandin synthesis by cyclooxygenases (COX). In this study, when PPARα agonist WY-14,643 was mixed in liquid Lieber-DeCarli ethanol or control diets and fed to mice, liver PLA2, COX-2, and ACOX1 were induced but ACSL4 was inhibited, suggesting that AA released by PLA2 from phospholipid will be metabolized to prostaglandin via COX-2 instead of being synthesized into acyl-CoA by ACSL4. However, liver prostaglandin E2 (PGE2), a major component of prostaglandin, was not increased with the induced COX-2 but decreased by WY-14,643. ACOX1 specific inhibitor mixed in the liquid diets restored both the WY-14,643-suppressed liver TG and PGE2, but COX-2 specific inhibitor celecoxib mixed in the liquid diets reversed the WY-14,643-suppressed liver TG but not liver PGE2 contents. These results suggest that induction of PLA2, COX-2 and ACOX1 orchestrates to increase oxidation of AA/PGE2, which constitutes one new mechanism by which PPARα induces peroxisomal FAO and inhibits ethanol-induced liver fat accumulation.
Keywords	acyl coenzyme A ; acyl-CoA oxidase ; agonists ; arachidonic acid ; beta oxidation ; esterification ; ethanol ; fatty liver ; liquids ; liver ; long-chain-fatty-acid-CoA ligase ; mitochondria ; oxidation ; peroxisomes ; phospholipase A2 ; phospholipids ; prostaglandin synthase ; prostaglandins ; research
Language	English
Dates of publication	2022-0712
Size	p. 47-52.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	205723-2
ISSN	0006-291X ; 0006-291X
ISSN (online)	0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2022.04.132
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Article ; Online: PPARα agonist WY-14,643 induces adipose atrophy and fails to blunt chronic ethanol-induced hepatic fat accumulation in mice lacking adipose FGFR1.

Xu, Yunhui / Denning, Krista L / Lu, Yongke

Biochemical pharmacology

2021 Volume 192, Page(s) 114678

Abstract: Fibroblast growth factor 21 (FGF21) is mainly regulated by peroxisome proliferator-activated receptor α (PPARα) in liver. The PPARα-FGF21 axis protects against alcohol-related liver disease (ALD). FGF21 exerts its effect via FGF receptor 1 (FGFR1). ... ...

Abstract	Fibroblast growth factor 21 (FGF21) is mainly regulated by peroxisome proliferator-activated receptor α (PPARα) in liver. The PPARα-FGF21 axis protects against alcohol-related liver disease (ALD). FGF21 exerts its effect via FGF receptor 1 (FGFR1). However, liver specific FGFR1 abrogation had no effect on ALD. Adipose tissues highly express FGFR1. When adipocyte specific FGFR1 knockout (fgfr1
MeSH term(s)	Adipose Tissue/drug effects ; Adipose Tissue/metabolism ; Animals ; Atrophy/chemically induced ; Atrophy/metabolism ; Ethanol/administration & dosage ; Ethanol/toxicity ; Fatty Liver, Alcoholic/metabolism ; Fatty Liver, Alcoholic/prevention & control ; Female ; Mice ; Mice, Knockout ; PPAR alpha/agonists ; PPAR alpha/metabolism ; Peroxisome Proliferators/therapeutic use ; Peroxisome Proliferators/toxicity ; Pyrimidines/therapeutic use ; Pyrimidines/toxicity ; Receptor, Fibroblast Growth Factor, Type 1/deficiency ; Receptor, Fibroblast Growth Factor, Type 1/genetics
Chemical Substances	PPAR alpha ; Peroxisome Proliferators ; Pyrimidines ; Ethanol (3K9958V90M) ; pirinixic acid (86C4MRT55A) ; Fgfr1 protein, mouse (EC 2.7.10.1) ; Receptor, Fibroblast Growth Factor, Type 1 (EC 2.7.10.1)
Language	English
Publishing date	2021-07-13
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	208787-x
ISSN	1873-2968 ; 0006-2952
ISSN (online)	1873-2968
ISSN	0006-2952
DOI	10.1016/j.bcp.2021.114678
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