Osteocalcin promotes bone mineralization but is not a hormone

About the Authors: Stavros C. Manolagas * E-mail: ManolagasStavros@uams.edu Affiliations Division of Endocrinology and Metabolism, Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences, Arkansas, United States of America, Central Arkansas Veterans Healthcar...

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Published in:PLoS genetics 2020-06, Vol.16 (6), p.e1008714-e1008714
Main Author: Manolagas, Stavros C
Format: Article
Language:English
Subjects:
Aging
Beta cells
Biology
Biology and Life Sciences
Bone diseases
Bone healing
Bone morphogenetic proteins
Bone tumors
Brain research
Calcification (Physiology)
Calcium
Cell proliferation
Collagen
Composition
Endocrinology
Energy metabolism
Fertility
Funding
Gene targeting
Genes
Genetic aspects
Genetics
Glucose
Glucose metabolism
Health aspects
Hydroxyapatite
Hyperparathyroidism
Hyperthyroidism
Hypoparathyroidism
Identification and classification
Lactation
Medicine and Health Sciences
Menopause
Menstrual cycle
Metabolism
Mineralization
Osteoblasts
Osteocalcin
Osteoporosis
Pancreas
Pregnancy
Research and Analysis Methods
Skeleton
Stem cells
Testosterone
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Summary:About the Authors: Stavros C. Manolagas * E-mail: ManolagasStavros@uams.edu Affiliations Division of Endocrinology and Metabolism, Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences, Arkansas, United States of America, Central Arkansas Veterans Healthcare System, Little Rock, Arkansas, United States of America ORCID logo http://orcid.org/0000-0002-0826-3484 Citation: Manolagas SC (2020) Osteocalcin promotes bone mineralization but is not a hormone. Examples are skeletal development, growth, adaptation of the skeleton to mechanical forces, fracture healing, changing calcium needs, stress, menstrual cycle, pregnancy, lactation, menopause, aging, hyperparathyroidism or hypoparathyroidism, hyperthyroidism, hypercortisolemia, Paget’s disease, bone tumors, etc. [...]mouse gene targeting studies of GPRC6A, proposed to be an OCN receptor that modulates pancreatic β-cell proliferation [3], have yielded conflicting results with regard to glucose and energy metabolism [9–11]. The mutant mice do, nonetheless, exhibit increased bone crystal size and maturation of hydroxyapatite, consistent with the aforementioned report of Moriishi and colleagues, earlier evidence by many other groups, and the general consensus that OCN plays a role in mineralization.
ISSN:1553-7404
1553-7390
1553-7404
DOI:10.1371/journal.pgen.1008714