Liver p53 is stabilized upon starvation and required for amino acid catabolism and gluconeogenesis.

ABSTRACT: The ability to adapt cellular metabolism to nutrient availability is critical for survival. The liver plays a central role in the adaptation to starvation by switching from glucose-consuming processes and lipid synthesis to providing energy substrates like glucose to the organism. Here we report a previously unrecognized role of the tumor suppressor p53 in the physiologic adaptation to food withdrawal. We found that starvation robustly increases p53 protein in mouse liver. This induction was posttranscriptional and mediated by a hepatocyte-autonomous and AMP-activated protein kinase-dependent mechanism. p53 stabilization was required for the adaptive expression of genes involved in amino acid catabolism. Indeed, acute deletion of p53 in livers of adult mice impaired hepatic glycogen storag

SUBMITTER: Prokesch A 

PROVIDER: S-EPMC5240663 | biostudies-literature | 2017 Feb

REPOSITORIES: biostudies-literature