Primary osteoblasts and osteoblast-like cells in culture bind insulin and respond to insulin treatment [5–7], as is evidenced by increased cell proliferation rates [8, 9], enhanced collagen synthesis [6, 10–12], secretion of bone formation markers [13], and increased uptake of glucose [14, 15]. In vivo, systemic insulin therapy can prevent or reverse skeletal deficits which occur in rodent models of T1D, including improving bone strength and biomechanical integrity [16–19]. This evidence concerns the gene INS and type 1 diabetes mellitus.