biostudies-literatureTadinada SMAmerican Heart AssociationBLRD VAHHS | NIH | NIH Office of the DirectorNHLBI NIH HHSHHS | NIH | National Heart, Lung, and Blood InstituteNCI NIH HHSNIH HHSH850-H864https://www.ebi.ac.uk/biostudies/studies/S-EPMC8616610biostudies-literatureUnknown321(5)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-laAmerican journal of physiology. Heart and circulatory physiologyFunctional resilience of C57BL/6J mouse heart to dietary fat overload.PMC8616610R01HL127764I01 BX004468S10OD019941P30 CA086862R01 HL142935R01 HL127764R01HL14293520SFRN35120123S10 OD019941P01 CA217797R01HL112413R01 HL112413O'Neill BTWeiss RMKutschke WWeatherford ETBosko AAbel EDCochran JCollins GVBhardwaj GZimmerman KTadinada SMfalseFunctional resilience of C57BL/6J mouse heart to dietary fat overload.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-la2021-01-01T00:00:00Z2021 Nov2025-04-04T22:33:01.386Z2025-02-19T03:23:56.778ZS-EPMC86166103447746110.1152/ajpheart.00419.2021