{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Abbas A"],"funding":["British Heart Foundation","Medical Research Council","Wellcome Trust"],"pagination":["2169-78"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3142083"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["60(8)"],"pubmed_abstract":["Objective
In mice, haploinsufficiency of the IGF-1 receptor (IGF-1R(+/-)), at a whole-body level, increases resistance to inflammation and oxidative stress, but the underlying mechanisms are unclear. We hypothesized that by forming insulin-resistant heterodimers composed of one IGF-1Rαβ and one insulin receptor (IR), IRαβ complex in endothelial cells (ECs), IGF-1R reduces free IR, which reduces EC insulin sensitivity and generation of the antioxidant/anti-inflammatory signaling radical nitric oxide (NO).Research design and methods
Using a number of complementary gene-modified mice with reduced IGF-1R at a whole-body level and specifically in EC, and complementary studies in EC in vitro, we examined the effect of changing IGF-1R/IR stoichiometry on EC insulin sensitivity and"],"journal":["Diabetes"],"pubmed_title":["The insulin-like growth factor-1 receptor is a negative regulator of nitric oxide bioavailability and insulin sensitivity in the endothelium."],"pmcid":["PMC3142083"],"funding_grant_id":["PG/09/042/27518","RG/07/003/23133","FS/10/028/28252","090532"],"pubmed_authors":["Beech DJ","Viswambharan H","Kearney MT","Gage M","Kahn M","Sukumar P","Imrie H","Rajwani A","Smith J","Channon KM","Wheatcroft SB","Cubbon RM","Xuan S","Abbas A","Galloway S","Yuldeshava N","Grant PJ"],"additional_accession":[]},"is_claimable":false,"name":"The insulin-like growth factor-1 receptor is a negative regulator of nitric oxide bioavailability and insulin sensitivity in the endothelium.","description":"Objective
In mice, haploinsufficiency of the IGF-1 receptor (IGF-1R(+/-)), at a whole-body level, increases resistance to inflammation and oxidative stress, but the underlying mechanisms are unclear. We hypothesized that by forming insulin-resistant heterodimers composed of one IGF-1Rαβ and one insulin receptor (IR), IRαβ complex in endothelial cells (ECs), IGF-1R reduces free IR, which reduces EC insulin sensitivity and generation of the antioxidant/anti-inflammatory signaling radical nitric oxide (NO).Research design and methods
Using a number of complementary gene-modified mice with reduced IGF-1R at a whole-body level and specifically in EC, and complementary studies in EC in vitro, we examined the effect of changing IGF-1R/IR stoichiometry on EC insulin sensitivity and","dates":{"release":"2011-01-01T00:00:00Z","publication":"2011 Aug","modification":"2025-04-04T12:00:43.518Z","creation":"2019-03-27T03:07:20Z"},"accession":"S-EPMC3142083","cross_references":{"pubmed":["21677284"],"doi":["10.2337/db11-0197"]}}