Please use this identifier to cite or link to this item:
Title: Insights into the role of hepatocyte PPARα activity in response to fasting
Authors: Régnier, Marion
Polizzi, Arnaud
Lippi, Yannick
Fouché, Edwin
Michel, Géraldine
Lukowicz, Céline
Smati, Sarra
Marrot, Alain
Lasserre, Frédéric
Naylies, Claire
Batut, Aurélie
Viars, Fanny
Bertrand-Michel, Justine
Postic, Catherine
Loiseau, Nicolas
Wahli, Walter
Guillou, Hervé
Montagner, Alexandra
Keywords: Science::Medicine
Issue Date: 2017
Source: Régnier, M., Polizzi, A., Lippi, Y., Fouché, E., Michel, G., Lukowicz, C., . . . Montagner, A. (2018). Insights into the role of hepatocyte PPARα activity in response to fasting. Molecular and Cellular Endocrinology, 471, 75-88. doi:10.1016/j.mce.2017.07.035
Journal: Molecular and Cellular Endocrinology
Abstract: The liver plays a central role in the regulation of fatty acid metabolism. Hepatocytes are highly sensitive to nutrients and hormones that drive extensive transcriptional responses. Nuclear hormone receptors are key transcription factors involved in this process. Among these factors, PPARα is a critical regulator of hepatic lipid catabolism during fasting. This study aimed to analyse the wide array of hepatic PPARα-dependent transcriptional responses during fasting. We compared gene expression in male mice with a hepatocyte specific deletion of PPARα and their wild-type littermates in the fed (ad libitum) and 24-h fasted states. Liver samples were acquired, and transcriptome and lipidome analyses were performed. Our data extended and confirmed the critical role of hepatocyte PPARα as a central for regulator of gene expression during starvation. Interestingly, we identified novel PPARα-sensitive genes, including Cxcl-10, Rab30, and Krt23. We also found that liver phospholipid remodelling was a novel fasting-sensitive pathway regulated by PPARα. These results may contribute to investigations on transcriptional control in hepatic physiology and underscore the clinical relevance of drugs that target PPARα in liver pathologies, such as non-alcoholic fatty liver disease.
ISSN: 0303-7207
DOI: 10.1016/j.mce.2017.07.035
Rights: © 2017 Elsevier B.V. All rights reserved.
Fulltext Permission: none
Fulltext Availability: No Fulltext
Appears in Collections:LKCMedicine Journal Articles

Citations 20

Updated on Jan 28, 2023

Web of ScienceTM
Citations 10

Updated on Jan 26, 2023

Page view(s)

Updated on Jan 28, 2023

Google ScholarTM




Items in DR-NTU are protected by copyright, with all rights reserved, unless otherwise indicated.