scholarly journals Intestinal peroxisomal fatty acid β-oxidation regulates neural serotonin signaling through a feedback mechanism

PLoS Biology ◽  
2019 ◽  
Vol 17 (12) ◽  
pp. e3000242 ◽  
Author(s):  
Aude D. Bouagnon ◽  
Lin Lin ◽  
Shubhi Srivastava ◽  
Chung-Chih Liu ◽  
Oishika Panda ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Feedback Mechanism ◽  
Serotonin Signaling ◽  
Peroxisomal Fatty Acid

Peroxisomal fatty acid alpha- and beta-oxidation in humans: new insights into enzymology, substrate specificities, metabolite transport and peroxisomal diseases

2001 ◽  
Vol 29 (1) ◽  
pp. A2-A2
Author(s):  
R. J. A. Wanders ◽  
S. Ferdinandusse ◽  
G. A. Jansen ◽  
E. G. van Grusven ◽  
H. R. Waterham ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Beta Oxidation ◽  
Metabolite Transport ◽  
Substrate Specificities ◽  
Peroxisomal Fatty Acid

Eicosapentaenoic and docosahexaenoic acid affect mitochondrial and peroxisomal fatty acid oxidation in relation to substrate preference

Lipids ◽  
1999 ◽  
Vol 34 (9) ◽  
pp. 951-963 ◽  
Author(s):  
Lise Madsen ◽  
Arild C. Rustan ◽  
Hege Vaagenes ◽  
Kjetil Berge ◽  
Endre Dyrøy ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Docosahexaenoic Acid ◽  
Fatty Acid Oxidation ◽  
Substrate Preference ◽  
Acid Oxidation ◽  
Peroxisomal Fatty Acid Oxidation ◽  
Peroxisomal Fatty Acid

Peroxisomal Fatty Acid β-Oxidation in Relation to Adrenoleukodystrophy

1991 ◽  
Vol 13 (4-5) ◽  
pp. 262-266 ◽  
Author(s):  
Ronald J.A. Wanders ◽  
Joseph M. Tager
Keyword(s):  
Fatty Acid ◽  
Peroxisomal Fatty Acid

scholarly journals Peroxisomal fatty acid oxidation and glycolysis are triggered in mouse models of lesional atopic dermatitis.

2021 ◽  
pp. 100033
Author(s):  
P. Pavel ◽  
G. Leman ◽  
M. Hermann ◽  
C. Ploner ◽  
T.O. Eichmann ◽  
...  
Keyword(s):  
Atopic Dermatitis ◽  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Mouse Models ◽  
Acid Oxidation ◽  
Peroxisomal Fatty Acid Oxidation ◽  
Peroxisomal Fatty Acid

An Increase in Peroxisomal Fatty Acid Oxidation Is Not Sufficient to Prevent Tissue Lipid Accumulation in hHTg Rats

2006 ◽  
Vol 967 (1) ◽  
pp. 71-79 ◽  
Author(s):  
J. UKROPEC ◽  
I. KLIMEŠ ◽  
D. GAŠPERÍKOVÁ ◽  
E. DEMCÁKOVÁ ◽  
C. A. DREVON ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Lipid Accumulation ◽  
Acid Oxidation ◽  
Tissue Lipid ◽  
Peroxisomal Fatty Acid Oxidation ◽  
Peroxisomal Fatty Acid

scholarly journals Redox, amino acid, and fatty acid metabolism intersect with bacterial virulence in the gut

2018 ◽  
Vol 115 (45) ◽  
pp. E10712-E10719 ◽  
Author(s):  
Reed Pifer ◽  
Regan M. Russell ◽  
Aman Kumar ◽  
Meredith M. Curtis ◽  
Vanessa Sperandio
Keyword(s):  
Fatty Acid ◽  
High Throughput ◽  
Fatty Acid Metabolism ◽  
Metabolic Pathways ◽  
Virulence Genes ◽  
Acid Metabolism ◽  
Feedback Mechanism ◽  
Regulatory Pathways ◽  
Successful Infection ◽  
Cellular Circuits

The gut metabolic landscape is complex and is influenced by the microbiota, host physiology, and enteric pathogens. Pathogens have to exquisitely monitor the biogeography of the gastrointestinal tract to find a suitable niche for colonization. To dissect the important metabolic pathways that influence virulence of enterohemorrhagicEscherichia coli(EHEC), we conducted a high-throughput screen. We generated a dataset of regulatory pathways that control EHEC virulence expression under anaerobic conditions. This unraveled that the cysteine-responsive regulator, CutR, converges with the YhaO serine import pump and the fatty acid metabolism regulator FadR to optimally control virulence expression in EHEC. CutR activates expression of YhaO to increase activity of the YhaJ transcription factor that has been previously shown to directly activate the EHEC virulence genes. CutR enhances FadL, which is a pump for fatty acids that represses inhibition of virulence expression by FadR, unmasking a feedback mechanism responsive to metabolite fluctuations. Moreover, CutR and FadR also augment murine infection byCitrobacter rodentium, which is a murine pathogen extensively employed as a surrogate animal model for EHEC. This high-throughput approach proved to be a powerful tool to map the web of cellular circuits that allows an enteric pathogen to monitor the gut environment and adjust the levels of expression of its virulence repertoire toward successful infection of the host.

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