{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Garcia-Caceres C"],"funding":["NIDDK NIH HHS"],"pagination":["867-880"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8961449"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["166(4)"],"pubmed_abstract":["We report that astrocytic insulin signaling co-regulates hypothalamic glucose sensing and systemic glucose metabolism. Postnatal ablation of insulin receptors (IRs) in glial fibrillary acidic protein (GFAP)-expressing cells affects hypothalamic astrocyte morphology, mitochondrial function, and circuit connectivity. Accordingly, astrocytic IR ablation reduces glucose-induced activation of hypothalamic pro-opio-melanocortin (POMC) neurons and impairs physiological responses to changes in glucose availability. Hypothalamus-specific knockout of astrocytic IRs, as well as postnatal ablation by targeting glutamate aspartate transporter (GLAST)-expressing cells, replicates such alterations. A normal response to altering directly CNS glucose levels in mice lacking astrocytic IRs indicates a role i"],"journal":["Cell"],"pubmed_title":["Astrocytic Insulin Signaling Couples Brain Glucose Uptake with Nutrient Availability."],"pmcid":["PMC8961449"],"funding_grant_id":["P30 DK036836","R01 DK031036"],"pubmed_authors":["Gotz M","Luquet S","Ninkovic J","Meyer CW","Gruber T","Le Thuc O","Fernandez AM","Garcia-Caceres C","Jastroch M","Yi CX","Woods SC","Varela L","Legutko B","Kahn CR","Szigeti-Buck K","Gao Y","Johansson P","Pfluger PT","Tschop MH","Quarta C","Cai W","Torres-Aleman I","Horvath TL"],"additional_accession":[]},"is_claimable":false,"name":"Astrocytic Insulin Signaling Couples Brain Glucose Uptake with Nutrient Availability.","description":"We report that astrocytic insulin signaling co-regulates hypothalamic glucose sensing and systemic glucose metabolism. Postnatal ablation of insulin receptors (IRs) in glial fibrillary acidic protein (GFAP)-expressing cells affects hypothalamic astrocyte morphology, mitochondrial function, and circuit connectivity. Accordingly, astrocytic IR ablation reduces glucose-induced activation of hypothalamic pro-opio-melanocortin (POMC) neurons and impairs physiological responses to changes in glucose availability. Hypothalamus-specific knockout of astrocytic IRs, as well as postnatal ablation by targeting glutamate aspartate transporter (GLAST)-expressing cells, replicates such alterations. A normal response to altering directly CNS glucose levels in mice lacking astrocytic IRs indicates a role i","dates":{"release":"2016-01-01T00:00:00Z","publication":"2016 Aug","modification":"2025-04-05T16:00:15.754Z","creation":"2025-04-05T16:00:15.754Z"},"accession":"S-EPMC8961449","cross_references":{"pubmed":["27518562"],"doi":["10.1016/j.cell.2016.07.028"]}}