{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Tadinada SM"],"funding":["American Heart Association","BLRD VA","HHS | NIH | NIH Office of the Director","NHLBI NIH HHS","HHS | NIH | National Heart, Lung, and Blood Institute","NCI NIH HHS","NIH HHS"],"pagination":["H850-H864"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8616610"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["321(5)"],"pubmed_abstract":["Molecular mechanisms underlying cardiac dysfunction and subsequent heart failure in diabetic cardiomyopathy are incompletely understood. Initially we intended to test the role of G protein-coupled receptor kinase 2 (GRK2), a potential mediator of cardiac dysfunction in diabetic cardiomyopathy, but found that control animals on HFD did not develop cardiomyopathy. Cardiac function was preserved in both wild-type and <i>GRK2</i> knockout animals fed high-fat diet as indicated by preserved left ventricular ejection fraction (LVEF) although heart mass was increased. The absence of cardiac dysfunction led us to rigorously evaluate the utility of diet-induced obesity to model diabetic cardiomyopathy in mice. Using pure C57BL/6J animals and various diets formulated with different sources of fat-la"],"journal":["American journal of physiology. Heart and circulatory physiology"],"pubmed_title":["Functional resilience of C57BL/6J mouse heart to dietary fat overload."],"pmcid":["PMC8616610"],"funding_grant_id":["R01HL127764","I01 BX004468","S10OD019941","P30 CA086862","R01 HL142935","R01 HL127764","R01HL142935","20SFRN35120123","S10 OD019941","P01 CA217797","R01HL112413","R01 HL112413"],"pubmed_authors":["O'Neill BT","Weiss RM","Kutschke W","Weatherford ET","Bosko A","Abel ED","Cochran J","Collins GV","Bhardwaj G","Zimmerman K","Tadinada SM"],"additional_accession":[]},"is_claimable":false,"name":"Functional resilience of C57BL/6J mouse heart to dietary fat overload.","description":"Molecular mechanisms underlying cardiac dysfunction and subsequent heart failure in diabetic cardiomyopathy are incompletely understood. Initially we intended to test the role of G protein-coupled receptor kinase 2 (GRK2), a potential mediator of cardiac dysfunction in diabetic cardiomyopathy, but found that control animals on HFD did not develop cardiomyopathy. Cardiac function was preserved in both wild-type and <i>GRK2</i> knockout animals fed high-fat diet as indicated by preserved left ventricular ejection fraction (LVEF) although heart mass was increased. The absence of cardiac dysfunction led us to rigorously evaluate the utility of diet-induced obesity to model diabetic cardiomyopathy in mice. Using pure C57BL/6J animals and various diets formulated with different sources of fat-la","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Nov","modification":"2025-04-04T22:33:01.386Z","creation":"2025-02-19T03:23:56.778Z"},"accession":"S-EPMC8616610","cross_references":{"pubmed":["34477461"],"doi":["10.1152/ajpheart.00419.2021"]}}