A. Polizzi

Discipline

Anthropologie biologique (1)

Type de document

Articles (10)

Co-auteur

Date

Source

Mot-clé

Liver (10) Mice (9) métabolisme (7) Metabolism (7) Metabolism (7) Genes (6) Animals (6) lipide (5) analyse (5) règlement (5) Deletion (5) Fasting (5) Regulation (5) Analysis (5) acide (4) Homeostasis (4) Glucose (4) Gene expression (4) puits (3) gène (3) maladie (3) Treatment (3) Fibroblast growth factors (3) Animal feeding (3) Transcription (3) Liver cells (3) Fatty liver (3) Fat (3) Diet (3) Fatty degeneration (3)

Documents écrit par A. Polizzi (10) | parle de A. Polizzi (0)

ATGL-dependent white adipose tissue lipolysis controls hepatocyte PPARα activity.
A. Fougerat et al. (7 juin 2022)
The hepatocyte insulin receptor is required to program the liver clock and rhythmic gene expression.
T. Fougeray et al. (12 avr. 2022)
Integrative study of diet-induced mouse models of NAFLD identifies PPARα as a sexually dimorphic drug target.
S. Smati et al.
Nuclear HMGB1 protects from nonalcoholic fatty liver disease through negative regulation of liver X receptor.
J. Personnaz et al. (25 mars 2022)
The pregnane X receptor drives sexually dimorphic hepatic changes in lipid and xenobiotic metabolism in response to gut microbiota in mice.
S.A. Barretto et al. (20 avr. 2021)
Hepatocyte-specific deletion of Pparα promotes NAFLD in the context of obesity.
M. Régnier et al. (16 avr. 2020)
A Specific ChREBP and PPARα Cross-Talk Is Required for the Glucose-Mediated FGF21 Response.
A. Iroz et al. (10 oct. 2017)
Hepatic Fasting-Induced PPARα Activity Does Not Depend on Essential Fatty Acids.
A. Polizzi et al. (24 avr. 2016)
Hepatic circadian clock oscillators and nuclear receptors integrate microbiome-derived signals.
A. Montagner et al. (16 févr. 2016)
Liver PPARα is crucial for whole-body fatty acid homeostasis and is protective against NAFLD.
A. Montagner et al. (2016)