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

Autoři: Takeshi Moriishi aff001;  Ryosuke Ozasa aff002;  Takuya Ishimoto aff002;  Takayoshi Nakano aff002;  Tomoka Hasegawa aff003;  Toshihiro Miyazaki aff001;  Wenguang Liu aff004;  Ryo Fukuyama aff006;  Yuying Wang aff004;  Hisato Komori aff004;  Xin Qin aff004;  Norio Amizuka aff003;  Toshihisa Komori aff004
Působiště autorů: Department of Cell Biology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan aff001;  Division of Materials and Manufacturing Science, Graduate School of Engineering, Osaka University, Suita, Osaka, Japan aff002;  Department of Developmental Biology of Hard Tissue, Division of Oral Health Science, Graduate School of Dental Medicine, Hokkaido University, Sapporo, Japan aff003;  Basic and Translational Research Center for Hard Tissue Disease, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan aff004;  Institute of Genetics and Cytology, Northeast Normal University, Changchun, China aff005;  Laboratory of Pharmacology, Hiroshima International University, Kure, Japan aff006;  College of Life and Environmental Science, Hangzhou Normal University, Hangzhou, China aff007
Vyšlo v časopise: Osteocalcin is necessary for the alignment of apatite crystallites, but not glucose metabolism, testosterone synthesis, or muscle mass. PLoS Genet 16(5): e32767. doi:10.1371/journal.pgen.1008586
Kategorie: Research Article
doi: https://doi.org/10.1371/journal.pgen.1008586


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 pancreas, testosterone synthesis in the testes, and muscle mass. We generated Ocn-deficient (Ocn–/–) mice by deleting Bglap and Bglap2. 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 the c-axis were normal in the Ocn–/–bone. However, the crystallographic orientation of the BAp c-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.

Klíčová slova:

Bone development – Collagens – Glucose – Glucose metabolism – Mouse models – Sperm – Testosterone – Femur


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