Analysis of Adrβ2_osb^−/− mice. (A) Specificity of α1(I) Collagen–Cre-driven deletion of Adrβ2 allele in bone. (B) Expression level of Adrβ2 protein in bone marrow–derived osteoblasts. (C) Bone histomorphometric analysis Adrβ2_osb^−/− mice at 24 wk of age (control, n = 11; Adrβ2_osb^−/−, n = 7). Mineralized bone matrix is stained in black by Von Kossa reagent. Histomorphometric parameters: BV/TV, bone volume over tissue volume; Ob.Nb/T.Ar, number of osteoblasts per trabecular area; Oc.S/T.Ar, osteoclast surface per trabecular area. (D) µCT analysis of control (n = 6) and Adrβ2_osb^−/− (n = 5) proximal tibiae at 24 wk of age. Ct.Th, cortical thickness. (E) Expression of phospho-CREB and total CREB after 28-d leptin ICV infusion at 12 wk of age. (F and G) Expression of various genes in control (n = 7) and Adrβ2_osb^−/− (n = 7) bone at 24 wk of age. (H) Serum CTx levels of control (n = 8) and Adrβ2_osb^−/− (n = 7) mice at 24 wk of age. (I–L) Bone histomorphometric analysis of 12-wk-old Adrβ2_osb^−/− mice after leptin ICV infusion shown as percentage compared with control mice treated with vehicle ICV infusion (control mice with vehicle ICV infusion, n = 9; control mice with leptin ICV infusion, n = 8; Adrβ2_osb^−/− mice with vehicle ICV infusion, n = 5; Adrβ2_osb^−/− mice with leptin ICV infusion, n = 5). (M) Bone histomorphometric analysis of 12-wk-old Adrβ2_osb^−/− mice after leptin ICV infusion. All experiments were performed independently at least twice, and representative data are shown. Results are shown as mean ± SEM. Statistical analysis was performed by Student’s t test. For all panels: *, P < 0.05.