Deletion of Rptor in Preosteoblasts Reveals a Role for the Mammalian Target of Rapamycin Complex 1 (mTORC1) Complex in Dietary‐Induced Changes to Bone Mass and Glucose Homeostasis in Female Mice

Abstract

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Bone controls browning of white adipose tissue and protects from diet-induced obesity through Schnurri-3-regulated SLIT2 secretion

“…Multiple organs and tissues work together to sense and respond to nutritional challenges to maintain normal systemic metabolic homeostasis. Previous studies have identi ed genetic alterations that concurrently regulate both bone volume and systemic energy homeostasis, such as SOST and mTORC1 9,10,13 . Clinical data on the association between osteoporotic/osteopetrotic diseases and adiposity/BMI further suggests a relationship between skeletal metabolism and systemic energy metabolism [27][28][29][30] .…”

“…In addition to these, bone forming osteoblasts in the skeleton have been suggested to affect adipose tissue and systemic energy metabolism through the secretion of bone derived hormones or "osteokines" 6 such as osteocalcin 7,8 . Also, loss of mTORC1 signaling in osteoblasts results in signi cantly decreased adiposity and protects mice from diet-induced-obesity (DIO) 9,10 . Interestingly, this effect occurred even in osteocalcin de cient mice 7 , arguing for the presence of undiscovered skeletal regulators of systemic energy metabolism 6,11 .…”