{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Osborn O"],"funding":["NICHD NIH HHS","NIDDK NIH HHS","NINDS NIH HHS"],"pagination":["2444-53"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3386820"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["122(7)"],"pubmed_abstract":["Obesity-induced inflammation is a key component of systemic insulin resistance, which is a hallmark of type 2 diabetes. A major driver of this inflammation/insulin resistance syndrome is the accumulation of proinflammatory macrophages in adipose tissue and liver. We found that the orphan GPCR Gpr21 was highly expressed in the hypothalamus and macrophages of mice and that whole-body KO of this receptor led to a robust improvement in glucose tolerance and systemic insulin sensitivity and a modest lean phenotype. The improvement in insulin sensitivity in the high-fat diet-fed (HFD-fed) Gpr21 KO mouse was traced to a marked reduction in tissue inflammation caused by decreased chemotaxis of Gpr21 KO macrophages into adipose tissue and liver. Furthermore, mice lacking macrophage expression of Gp"],"journal":["The Journal of clinical investigation"],"pubmed_title":["G protein-coupled receptor 21 deletion improves insulin sensitivity in diet-induced obese mice."],"pmcid":["PMC3386820"],"funding_grant_id":["U54 HD012303","P30 NS047101","R01 DK033651","U54 HD 012303-25","P50 HD012303","P30 DK063491","DK063491","DK033651","R37 DK033651","P01 DK074868","DK074868"],"pubmed_authors":["Sanchez-Alavez M","Kim JJ","Thiede L","Li P","Osborn O","Scadeng M","Lu M","Heinrichsdorff J","Hadcock J","Olefsky JM","Nalbandian S","Oh DY","Talukdar S","Ofrecio JM","Schenk S","Bartfai T","Morinaga H","McNelis J"],"additional_accession":[]},"is_claimable":false,"name":"G protein-coupled receptor 21 deletion improves insulin sensitivity in diet-induced obese mice.","description":"Obesity-induced inflammation is a key component of systemic insulin resistance, which is a hallmark of type 2 diabetes. A major driver of this inflammation/insulin resistance syndrome is the accumulation of proinflammatory macrophages in adipose tissue and liver. We found that the orphan GPCR Gpr21 was highly expressed in the hypothalamus and macrophages of mice and that whole-body KO of this receptor led to a robust improvement in glucose tolerance and systemic insulin sensitivity and a modest lean phenotype. The improvement in insulin sensitivity in the high-fat diet-fed (HFD-fed) Gpr21 KO mouse was traced to a marked reduction in tissue inflammation caused by decreased chemotaxis of Gpr21 KO macrophages into adipose tissue and liver. Furthermore, mice lacking macrophage expression of Gp","dates":{"release":"2012-01-01T00:00:00Z","publication":"2012 Jul","modification":"2025-04-05T13:20:23.8Z","creation":"2019-03-27T00:55:05Z"},"accession":"S-EPMC3386820","cross_references":{"pubmed":["22653059"],"doi":["10.1172/JCI61953","10.1172/jci61953"]}}