This reduction in OB insulin signaling was also observed in other primary insulin target tissues such as liver, skeletal muscle, and adipose tissues.(25) To investigate if insulin resistance in bone is associated with hyperactivation of mTORC1, we fed wild‐type mice an obesogenic HFD for 12 weeks (from 4 to 16 weeks of age) and measured the basal phosphorylation levels of ribosomal S6 (rpS6 Ser240/244), a substrate for p70S6K, a primary mTORC1 effector,(35) as a readout of mTORC1 activity. This evidence concerns the gene RPS6 and Insulin resistance.