The mTORC1 complex in pre-osteoblasts regulates whole-body energy metabolism independently of osteocalcin.

ABSTRACT: Overnutrition causes hyperactivation of mTORC1-dependent negative feedback loops leading to the downregulation of insulin signaling and development of insulin resistance. In osteoblasts (OBs), insulin signaling plays a crucial role in the control of systemic glucose homeostasis. We utilized mice with conditional deletion of Rptor to investigate how the loss of mTORC1 function in OB affects glucose metabolism under normal and overnutrition dietary states. Compared to the controls, chow-fed Rptor_ob^-/- mice had substantially less fat mass and exhibited adipocyte hyperplasia. Remarkably, upon feeding with high-fat diet, mice with pre- and post-natal deletion of Rptor in OBs were protected from diet-induced obesity and exhibited improved glucose metabolism with lower fasti

SUBMITTER: Tangseefa P 

PROVIDER: S-EPMC7868369 | biostudies-literature | 2021 Feb

REPOSITORIES: biostudies-literature