Insulin Receptor Signaling in Osteoblasts Regulates Postnatal Bone Acquisition and Body Composition

(Cell 142, 309–319; July 23, 2010) In the original version of this paper, the authors neglected to acknowledge the contributions of Dr. Mathieu Ferron, who assayed osteocalcin levels in blinded samples (described in Figure 4) and assisted in performing the osteocalcin infusion studies (described in Figure 5). An edited version of the acknowledgments is included below, and the authors apologize for any inconvenience this may have caused. We are grateful for the assistance of the Small Animal Phenotyping Core and Metabolism Core Laboratory at the University of Alabama at Birmingham. We thank Dr. D. Accili for providing the tTR-IRKO mice and Dr. M. Bouxsein for assistance in analyzing the skeletal phenotype by micro-CT. We thank Dr. M. Ferron who provided osteocalcin measurements in serum and media samples and assisted in performing the osteocalcin infusion studies described in Figure 5. We also thank Drs. T. Nagy and T. Garvey for helpful suggestions during the completion of this work. Support was provided by a Merit Review Grant from the Veterans Administration (T.L.C.) and grants from the NIH (M.H., DK081472), the Baltimore Diabetes Research and Training Center (M.H., DK079637), and DFG (J.C.B., Br1492/7-1). T.L.C. is also the recipient of a Research Career Scientist Award from the Veterans Administration. Insulin Receptor Signaling in Osteoblasts Regulates Postnatal Bone Acquisition and Body CompositionFulzele et al.CellJuly 23, 2010In BriefGlobal energy balance in mammals is controlled by the actions of circulating hormones that coordinate fuel production and utilization in metabolically active tissues. Bone-derived osteocalcin, in its undercarboxylated, hormonal form, regulates fat deposition and is a potent insulin secretagogue. Here, we show that insulin receptor (IR) signaling in osteoblasts controls osteoblast development and osteocalcin expression by suppressing the Runx2 inhibitor Twist2. Mice lacking IR in osteoblasts have low circulating undercarboxylated osteocalcin and reduced bone acquisition due to decreased bone formation and deficient numbers of osteoblasts. Full-Text PDF Open Archive