<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Thrailkill K</submitter><funding>NIDDK NIH HHS</funding><funding>NCRR NIH HHS</funding><funding>National Institutes of Health</funding><pagination>703589</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4052184</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>2014</volume><pubmed_abstract>Type 1 diabetes mellitus (T1D) is associated with decreased bone mineral density, a deficit in bone structure, and subsequently an increased risk of fragility fracture. These clinical observations, paralleled by animal models of T1D, suggest that the insulinopenia of T1D has a deleterious effect on bone. To further examine the action of insulin signaling on bone development, we generated mice with an osteoprogenitor-selective (osterix-Cre) ablation of the insulin receptor (IR), designated OIRKO. OIRKO mice exhibited an 80% decrease in IR in osteoblasts. Prenatal elimination of IR did not affect fetal survival or gross morphology. However, loss of IR in mouse osteoblasts resulted in a postnatal growth-constricted phenotype. By 10-12 weeks of age, femurs of OIRKO mice were more slender, with</pubmed_abstract><journal>Journal of diabetes research</journal><pubmed_title>Loss of insulin receptor in osteoprogenitor cells impairs structural strength of bone.</pubmed_title><pmcid>PMC4052184</pmcid><funding_grant_id>C06 RR016517</funding_grant_id><funding_grant_id>R01 DK084045</funding_grant_id><funding_grant_id>C06RR16517</funding_grant_id><funding_grant_id>36112</funding_grant_id><funding_grant_id>R56 DK084045</funding_grant_id><pubmed_authors>Cockrell G</pubmed_authors><pubmed_authors>Lumpkin C</pubmed_authors><pubmed_authors>Morris L</pubmed_authors><pubmed_authors>Kahn CR</pubmed_authors><pubmed_authors>Fowlkes J</pubmed_authors><pubmed_authors>Bunn RC</pubmed_authors><pubmed_authors>Thrailkill K</pubmed_authors><pubmed_authors>Nyman JS</pubmed_authors><pubmed_authors>Wahl E</pubmed_authors></additional><is_claimable>false</is_claimable><name>Loss of insulin receptor in osteoprogenitor cells impairs structural strength of bone.</name><description>Type 1 diabetes mellitus (T1D) is associated with decreased bone mineral density, a deficit in bone structure, and subsequently an increased risk of fragility fracture. These clinical observations, paralleled by animal models of T1D, suggest that the insulinopenia of T1D has a deleterious effect on bone. To further examine the action of insulin signaling on bone development, we generated mice with an osteoprogenitor-selective (osterix-Cre) ablation of the insulin receptor (IR), designated OIRKO. OIRKO mice exhibited an 80% decrease in IR in osteoblasts. Prenatal elimination of IR did not affect fetal survival or gross morphology. However, loss of IR in mouse osteoblasts resulted in a postnatal growth-constricted phenotype. By 10-12 weeks of age, femurs of OIRKO mice were more slender, with</description><dates><release>2014-01-01T00:00:00Z</release><publication>2014</publication><modification>2025-04-21T18:55:36.041Z</modification><creation>2019-03-27T01:29:51Z</creation></dates><accession>S-EPMC4052184</accession><cross_references><pubmed>24963495</pubmed><doi>10.1155/2014/703589</doi></cross_references></HashMap>