Importantly, these mice are protected from HFD‐induced marrow adiposity expansion, obesity, and insulin resistance, suggesting an important role for the mTORC1 pathway in the skeletal regulation of glucose metabolism, and providing strong evidence to support the concept that dysregulated insulin signaling in OBs has systemic effects on glucoregulation and energy homeostasis. This evidence concerns the gene INS and obesity due to melanocortin 4 receptor deficiency.