{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Dumolt JH"],"funding":["Eunice Kennedy Shriver National Institute of Child Health and Human Development","NICHD NIH HHS","HHS | NIH | Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD)"],"pagination":["e70100"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11508969"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["38(19)"],"pubmed_abstract":["Maternal obesity in pregnancy is strongly associated with complications such as fetal overgrowth and infants of obese mothers have an increased risk to develop obesity, diabetes, and cardiovascular disease later in life. However, the underlying mechanisms are not well established. Circulating levels of adiponectin are low in obese pregnant women and maternal circulating adiponectin is negatively associated with birth weight. We have reported that normalizing maternal adiponectin in obese pregnant mice prevents placental dysfunction, fetal overgrowth, and programming of offspring cardio-metabolic disease. However, the mechanistic link between maternal adiponectin, placental function, and fetal growth remains to be established. We hypothesized that trophoblast-specific overexpression of the "],"journal":["FASEB journal : official publication of the Federation of American Societies for Experimental Biology"],"pubmed_title":["Trophoblast-specific overexpression of adiponectin receptor 2 causes fetal growth restriction in pregnant mice."],"pmcid":["PMC11508969"],"funding_grant_id":["HD065007","T32 HD007186","HD007186","R01 HD105701","R01 HD065007","R01 HD068370","HD068370"],"pubmed_authors":["Barentsen K","Jansson T","Dumolt JH","Urschitz J","Powell TL","Rosario FJ"],"additional_accession":[]},"is_claimable":false,"name":"Trophoblast-specific overexpression of adiponectin receptor 2 causes fetal growth restriction in pregnant mice.","description":"Maternal obesity in pregnancy is strongly associated with complications such as fetal overgrowth and infants of obese mothers have an increased risk to develop obesity, diabetes, and cardiovascular disease later in life. However, the underlying mechanisms are not well established. Circulating levels of adiponectin are low in obese pregnant women and maternal circulating adiponectin is negatively associated with birth weight. We have reported that normalizing maternal adiponectin in obese pregnant mice prevents placental dysfunction, fetal overgrowth, and programming of offspring cardio-metabolic disease. However, the mechanistic link between maternal adiponectin, placental function, and fetal growth remains to be established. We hypothesized that trophoblast-specific overexpression of the ","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Oct","modification":"2026-06-04T10:55:24.749Z","creation":"2026-05-08T03:10:34.822Z"},"accession":"S-EPMC11508969","cross_references":{"pubmed":["39387608"],"doi":["10.1096/fj.202302143R","10.1096/fj.202302143r"]}}