Data

Data from: Chronic activation of PPARα with fenofibrate reduces autophagic proteins in the liver of mice independent of FGF21

RMIT University, Australia
Professor Jiming Ye (Associated with, Aggregated by)
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ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Adc&rfr_id=info%3Asid%2FANDS&rft_id=https://figshare.com/articles/Chronic_activation_of_PPAR_with_fenofibrate_reduces_autophagic_proteins_in_the_liver_of_mice_independent_of_FGF21/4889369&rft.title=Data from: Chronic activation of PPARα with fenofibrate reduces autophagic proteins in the liver of mice independent of FGF21&rft.identifier=cbc1b35a06189d396bb02496272ee47b&rft.publisher=RMIT University, Australia&rft.description=Attached file provides supplementary data for linked article. Autophagy is a catabolic mechanism to degrade cellular components to maintain cellular energy levels during starvation, a condition where PPARα may be activated. Here we report a reduced autophagic capacity in the liver following chronic activation of PPARα with fenofibrate (FB) in mice. Chronic administration of the PPARα agonist FB substantially reduced the levels of multiple autophagy proteins in the liver (Atg3, Agt4B, Atg5, Atg7 and beclin 1) which were associated with a decrease in the light chain LC3II/LC3I ratio and the accumulation of p62. This was concomitant with an increase in the expression of lipogenic proteins mSREBP1c, ACC, FAS and SCD1. These effects of FB were completely abolished in PPARα-/- mice but remained intact in mice with global deletion of FGF21, a key downstream mediator for PPARα-induced effects. Further studies showed that decreased the content of autophagy proteins by FB was associated with a significant reduction in the level of FoxO1, a transcriptional regulator of autophagic proteins, which occurred independently of both mTOR and Akt. These findings suggest that chronic stimulation of PPARα may suppress the autophagy capacity in the liver as a result of reduced content of a number of autophagyassociated proteins independent of FGF21.&rft.creator=Professor Jiming Ye&rft.date=2018&rft.relation=https://dx.doi.org/10.1371/journal.pone.0173676&rft_rights=Further information about rights and usage of ACS publications and supplementary data can be found here: http://pubs.acs.org/page/copyright/permissions.html.&rft_rights=CC BY-NC: Attribution-Noncommercial 3.0 AU http://creativecommons.org/licenses/by-nc/3.0/au&rft_subject=Insulin signaling transduction &rft_subject=Glucose-homeostasis&rft_subject=Fibroblast-growth-factor-21 &rft_subject=Deacetylation&rft_subject=Metabolism &rft_subject=Resistance&rft_subject=Steatosis&rft_subject=Receptors&rft_subject=Metabolic Medicine&rft_subject=MEDICAL AND HEALTH SCIENCES&rft_subject=MEDICAL BIOCHEMISTRY AND METABOLOMICS&rft.type=dataset&rft.language=English Access the data
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Attached file provides supplementary data for linked article. Autophagy is a catabolic mechanism to degrade cellular components to maintain cellular energy levels during starvation, a condition where PPARα may be activated. Here we report a reduced autophagic capacity in the liver following chronic activation of PPARα with fenofibrate (FB) in mice. Chronic administration of the PPARα agonist FB substantially reduced the levels of multiple autophagy proteins in the liver (Atg3, Agt4B, Atg5, Atg7 and beclin 1) which were associated with a decrease in the light chain LC3II/LC3I ratio and the accumulation of p62. This was concomitant with an increase in the expression of lipogenic proteins mSREBP1c, ACC, FAS and SCD1. These effects of FB were completely abolished in PPARα-/- mice but remained intact in mice with global deletion of FGF21, a key downstream mediator for PPARα-induced effects. Further studies showed that decreased the content of autophagy proteins by FB was associated with a significant reduction in the level of FoxO1, a transcriptional regulator of autophagic proteins, which occurred independently of both mTOR and Akt. These findings suggest that chronic stimulation of PPARα may suppress the autophagy capacity in the liver as a result of reduced content of a number of autophagyassociated proteins independent of FGF21.

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Deacetylation | Fibroblast-growth-factor-21 | Glucose-homeostasis | Insulin signaling transduction | Medical and Health Sciences | Medical Biochemistry and Metabolomics | Metabolic Medicine | Metabolism | Receptors | Resistance | Steatosis |

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  • Local : cbc1b35a06189d396bb02496272ee47b
ACN 633 798 857