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Regulation of energy metabolism by the skeleton: Osteocalcin and beyond
Abstract
The skeleton has recently emerged as an endocrine organ implicated in the regulation of glucose and energy metabolism. This function of bone is mediated, at least in part, by osteocalcin, an osteoblast-derived protein acting as a hormone stimulating insulin sensitivity, insulin secretion and energy expenditure. Osteocalcin secretion and bioactivity is in turn regulated by several hormonal cues including insulin, leptin, the sympathetic nervous system and glucocorticoids. Recent findings support the notion that osteocalcin functions and regulations are conserved between mice and humans. Moreover, studies in mice suggest that osteocalcin could represent a viable therapeutic approach for the treatment of obesity and insulin resistance. In this review, we summarize the current knowledge on osteocalcin functions, its various modes of action and the mechanisms implicated in the control of this hormone.
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“From % to % of patients with endogenous CS have DM, and % to % have defective glucose tolerance, so the overall prevalence of glucose metabolism impairments can come close to %, as shown in Table (, , -).”
From Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management (2017) · cites this paper as [143]
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Metadata
- Authors
- Ferron, M., & Lacombe, J.
- Affiliations
- Montreal Clinical Research Institute (CA)
- Corresponding author
- Ferron, Mathieu
- Venue
- Archives of Biochemistry and Biophysics
- Publisher
- Elsevier BV
- Published
- 2014-11
- Volume
- 561
- Pages
- 137-146
- ISSN
- 0003-9861 (ISSN-L)
- OpenAlex
- W2048096271
- Cited by
- 211
- References
- 179
- Citations by year
- 2026: 5 · 2025: 12 · 2024: 15 · 2023: 21 · 2022: 17 · 2021: 16 · 2020: 21 · 2019: 16 · 2018: 20 · 2017: 24 · 2016: 19 · 2015: 19 · 2014: 5
- FWCI
- 2.10
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Archives of Biochemistry and Biophysics (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Canadian Institutes of Health Research
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Orthopedics and Sports Medicine › Bone health and osteoporosis research
- Keywords
- osteocalcin, bone endocrine function, energy metabolism, glucose metabolism, insulin sensitivity, insulin secretion, energy expenditure, leptin, sympathetic nervous system, glucocorticoids, obesity, insulin resistance, osteoblasts, therapeutic target
- MeSH terms
- Animals, Bone and Bones, Energy Metabolism, Glucose, Homeostasis, Humans, Insulin, Insulin Resistance, Osteocalcin, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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