Postnatal loss of the insulin receptor in osteoprogenitor cells does not impart a metabolic phenotype.
Animals
Body Composition
Body Weight
Female
Glucose Tolerance Test
Glycated Hemoglobin
/ analysis
Insulin
/ metabolism
Islets of Langerhans
/ metabolism
Male
Metabolic Diseases
/ metabolism
Mice
Mice, Inbred C57BL
Mice, Transgenic
Osteocalcin
/ genetics
Phenotype
Receptor, Insulin
/ deficiency
Stem Cells
/ cytology
Journal
Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288
Informations de publication
Date de publication:
01 06 2020
01 06 2020
Historique:
received:
02
03
2020
accepted:
07
05
2020
entrez:
3
6
2020
pubmed:
3
6
2020
medline:
27
11
2020
Statut:
epublish
Résumé
The relationship between osteoblast-specific insulin signaling, osteocalcin activation and gluco-metabolic homeostasis has proven to be complex and potentially inconsistent across animal-model systems and in humans. Moreover, the impact of postnatally acquired, osteoblast-specific insulin deficiency on the pancreas-to-skeleton-to-pancreas circuit has not been studied. To explore this relationship, we created a model of postnatal elimination of insulin signaling in osteoprogenitors. Osteoprogenitor-selective ablation of the insulin receptor was induced after ~10 weeks of age in IR
Identifiants
pubmed: 32483283
doi: 10.1038/s41598-020-65717-3
pii: 10.1038/s41598-020-65717-3
pmc: PMC7264347
doi:
Substances chimiques
Glycated Hemoglobin A
0
Insulin
0
Osteocalcin
104982-03-8
Receptor, Insulin
EC 2.7.10.1
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
8842Subventions
Organisme : NIDDK NIH HHS
ID : R01 DK084045
Pays : United States
Organisme : NIAMS NIH HHS
ID : R21 AR070620
Pays : United States
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