New Work from Pajvani with a Model of Raptor-PHLPP2 Signaling

In normal/healthy liver, mTORC1-independent (”free”) Raptor stabilizes PHLPP2 to terminate Akt action. Aging or obesity reduces Raptorfree, leading to PHLPP2 degradation and prolonged Akt action, increasing de novo lipogenesis (DNL) and fatty liver. Hepatic glucose production (HGP) is also increased by insulin resistance, but is unaffected by the Raptorfree-PHLPP2 axis.

Read the article: "Free" Raptor - a novel regulator of metabolism.