Moreover, osteoblasts express GLUT4, an insulin dependent glucose transporter, and its deletion in osteoblasts from in vitro experiments results in impaired insulin stimulated glucose uptake, while in vivo, osteoblast specific GLUT4 knockout mice (ΔGlut4) displayed hyperinsulinemia, insulin resistance, and increased peripheral fat deposition (177). Here, SLC2A4 is linked to hyperinsulinism.