{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Reilly AM"],"funding":["U.S. Department of Health &amp; Human Services | NIH | National Center for Advancing Translational Sciences","NIDDK NIH HHS","Paul and Carole Stark Fellowship","U.S. Department of Health &amp; Human Services | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (National Institute of Diabetes &amp; Digestive &amp; Kidney Diseases)","U.S. Department of Health &amp; Human Services | NIH | National Center for Advancing Translational Sciences (NCATS)","U.S. Department of Health &amp; Human Services | NIH | National Institute of Diabetes and Digestive and Kidney Diseases"],"pagination":["29"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6791877"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["9(1)"],"pubmed_abstract":["<h4>Background</h4>Proopiomelanocortin (POMC) neurons in the arcuate nucleus of the hypothalamus (ARH) control energy homeostasis by sensing hormonal and nutrient cues and activating secondary melanocortin sensing neurons. We identified the expression of a G protein-coupled receptor, Gpr17, in the ARH and hypothesized that it contributes to the regulatory function of POMC neurons on metabolism.<h4>Methods</h4>In order to test this hypothesis, we generated POMC neuron-specific Gpr17 knockout (PGKO) mice and determined their energy and glucose metabolic phenotypes on normal chow diet (NCD) and high-fat diet (HFD).<h4>Results</h4>Adult PGKO mice on NCD displayed comparable body composition and metabolic features measured by indirect calorimetry. By contrast, PGKO mice on HFD demonstrated a se"],"journal":["Nutrition & diabetes"],"pubmed_title":["Gpr17 deficiency in POMC neurons ameliorates the metabolic derangements caused by long-term high-fat diet feeding."],"pmcid":["PMC6791877"],"funding_grant_id":["R00 DK098294","T32 DK064466","P30DK97512","R00DK09824","P30 DK097512","UL1TR002529"],"pubmed_authors":["Ren H","Wardlaw SL","Zhou S","Panigrahi SK","Sheets PL","Yan S","Reilly AM","Conley JM"],"additional_accession":[]},"is_claimable":false,"name":"Gpr17 deficiency in POMC neurons ameliorates the metabolic derangements caused by long-term high-fat diet feeding.","description":"<h4>Background</h4>Proopiomelanocortin (POMC) neurons in the arcuate nucleus of the hypothalamus (ARH) control energy homeostasis by sensing hormonal and nutrient cues and activating secondary melanocortin sensing neurons. We identified the expression of a G protein-coupled receptor, Gpr17, in the ARH and hypothesized that it contributes to the regulatory function of POMC neurons on metabolism.<h4>Methods</h4>In order to test this hypothesis, we generated POMC neuron-specific Gpr17 knockout (PGKO) mice and determined their energy and glucose metabolic phenotypes on normal chow diet (NCD) and high-fat diet (HFD).<h4>Results</h4>Adult PGKO mice on NCD displayed comparable body composition and metabolic features measured by indirect calorimetry. By contrast, PGKO mice on HFD demonstrated a se","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 Oct","modification":"2026-05-07T06:00:46.531Z","creation":"2019-10-30T08:22:20Z"},"accession":"S-EPMC6791877","cross_references":{"pubmed":["31611548"],"doi":["10.1038/s41387-019-0096-7"]}}