Metabolic phenotype in the mouse model of osteogenesis imperfecta

• Published in: Journal of endocrinology Vol. 234; no. 3; pp. 279 - 289
• Main Authors: Boraschi-Diaz, Iris, Tauer, Josephine T, El-Rifai, Omar, Guillemette, Delphine, Lefebvre, Geneviève, Rauch, Frank, Ferron, Mathieu, Komarova, Svetlana V
• Format: Journal Article
• Language: English
• Published: England Bioscientifica Ltd 01.09.2017; Portland Press Ltd The Biochemical Society
• Subjects: Adipose tissue; Animals; Bone growth; Bone resorption; Calorimetry; Carbon dioxide; Collagen (type I); Collagen Type I - genetics; Collagen Type I - metabolism; Disease Models, Animal; Energy expenditure; Energy metabolism; Female; Genotype & phenotype; Glucose tolerance; Hereditary diseases; Homeostasis; Humans; Insulin; Insulin secretion; Male; Metabolism; Mice; Mutation; Osteocalcin; Osteocalcin - genetics; Osteocalcin - metabolism; Osteogenesis; Osteogenesis imperfecta; Osteogenesis Imperfecta - genetics; Osteogenesis Imperfecta - metabolism; Phenotype; Rodents; Secretion; glucose homeostasis; undercarboxylated osteocalcin; metabolism; osteogenesis imperfecta; indirect calorimetry

Osteogenesis imperfecta (OI) is the most common heritable bone fragility disorder, usually caused by dominant mutations in genes coding for collagen type I alpha chains, COL1A1 or COL1A2. Osteocalcin (OCN) is now recognized as a bone-derived regulator of insulin secretion and sensitivity and glucose...