{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Huang Y"],"funding":["Natural Sciences and Engineering Research Council of Canada","Research and Development Corporation of Newfoundland and Labrador","China Scholarship Council","NCATS NIH HHS","National Institutes of Health","NIAMS NIH HHS","Canadian Institutes of Health Research","Newfoundland and Labrador"],"pagination":["106923"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10239698"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["26(6)"],"pubmed_abstract":["While insulin resistance (IR) is associated with inflammation in white adipose tissue, we report a non-inflammatory adipose mechanism of high fat-induced IR mediated by loss of Pref-1. Pref-1, released from adipose Pref-1+ cells with characteristics of M2 macrophages, endothelial cells or progenitors, inhibits MIF release from both Pref-1+ cells and adipocytes by binding with integrin β1 and inhibiting the mobilization of p115. High palmitic acid induces PAR2 expression in Pref-1+ cells, downregulating Pref-1 expression and release in an AMPK-dependent manner. The loss of Pref-1 increases adipose MIF secretion contributing to non-inflammatory IR in obesity. Treatment with Pref-1 blunts the increase in circulating plasma MIF levels and subsequent IR induced by a high palmitic acid diet. Thu"],"journal":["iScience"],"pubmed_title":["A pref-1-controlled non-inflammatory mechanism of insulin resistance."],"pmcid":["PMC10239698"],"funding_grant_id":["RDC 5404.1980.102","RGPIN-2017-04542","R01 AR078334","UL1 TR001863","AR-078334","PJT-156116"],"pubmed_authors":["Muller GK","Xia Z","Young LH","Fifield KE","Chen L","Bucala R","McGuire J","Liu S","Leng L","Xu J","Wu H","Wang L","Vanderluit JL","Huang Y","Wang S","Qi Y","Tong H","Qi D","Gao X","Sun G","Cui D"],"additional_accession":[]},"is_claimable":false,"name":"A pref-1-controlled non-inflammatory mechanism of insulin resistance.","description":"While insulin resistance (IR) is associated with inflammation in white adipose tissue, we report a non-inflammatory adipose mechanism of high fat-induced IR mediated by loss of Pref-1. Pref-1, released from adipose Pref-1+ cells with characteristics of M2 macrophages, endothelial cells or progenitors, inhibits MIF release from both Pref-1+ cells and adipocytes by binding with integrin β1 and inhibiting the mobilization of p115. High palmitic acid induces PAR2 expression in Pref-1+ cells, downregulating Pref-1 expression and release in an AMPK-dependent manner. The loss of Pref-1 increases adipose MIF secretion contributing to non-inflammatory IR in obesity. Treatment with Pref-1 blunts the increase in circulating plasma MIF levels and subsequent IR induced by a high palmitic acid diet. Thu","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Jun","modification":"2026-05-05T02:53:14.147Z","creation":"2025-04-04T07:59:28.744Z"},"accession":"S-EPMC10239698","cross_references":{"pubmed":["37283810"],"doi":["10.1016/j.isci.2023.106923"]}}