MTORC1 activation is not sufficient to suppress hepatic PPARα signaling or ketogenesis.

ABSTRACT: The mechanistic target of rapamycin (mTOR) is often referred to as a master regulator of the cellular metabolism that can integrate the growth factor and nutrient signaling. Fasting suppresses hepatic mTORC1 activity via the activity of the tuberous sclerosis complex (TSC), a negative regulator of mTORC1, to suppress anabolic metabolism. The loss of TSC1 in the liver locks the liver in a constitutively anabolic state even during fasting, which was suggested to regulate peroxisome proliferator-activated receptor alpha (PPARα) signaling and ketogenesis, but the molecular determinants of this regulation are unknown. Here, we examined if the activation of the mTORC1 complex in mice by the liver-specific deletion of TSC1 (TSC1^L-/-) is sufficient to suppress PPARα signaling and theref

SUBMITTER: Selen ES 

PROVIDER: S-EPMC8294577 | biostudies-literature | 2021 Jul

REPOSITORIES: biostudies-literature