Osteocalcin is necessary for the alignment of apatite crystallites, but not glucose metabolism, testosterone synthesis, or muscle mass

by Takeshi Moriishi, Ryosuke Ozasa, Takuya Ishimoto, Takayoshi Nakano, Tomoka Hasegawa, Toshihiro Miyazaki, Wenguang Liu, Ryo Fukuyama, Yuying Wang, Hisato Komori, Xin Qin, Norio Amizuka, Toshihisa Komori The strength of bone depends on bone quantity and quality. Osteocalcin (Ocn) is the most abundant noncollagenous protein in bone and is produced by osteoblasts. It has been previously claimed that Ocn inhibits bone formation and also functions as a hormone to regulate insulin secretion in the panc reas, testosterone synthesis in the testes, and muscle mass. We generated Ocn-deficient (Ocn–/–) mice by deletingBglap andBglap2. Analysis of Ocn–/–mice revealed that Ocn is not involved in the regulation of bone quantity, glucose metabolism, testosterone synthesis, or muscle mass. The orientation degree of collagen fibrils and size of biological apatite (BAp) crystallites in thec-axis were normal in the Ocn–/–bone. However, the crystallographic orientation of the BApc-axis, which is normally parallel to collagen fibrils, was severely disrupted, resulting in reduced bone strength. These results demonstrate that Ocn is required for bone quality and strength by adjusting the alignment of BAp crystallites parallel to collagen fibrils; but it does not function as a hormone.
Source: PLoS Genetics - Category: Genetics & Stem Cells Authors: Source Type: research
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