Oral 
diastolic dysfunction
DIASTOLIC DYSFUNCTION, OBESE
Following the observation of GGA‐induced attenuation of early diastolic dysfunction in obese ZSF1 rats, we conducted protein and cardiomyocyte function analyses to investigate the underlying mechanisms in cardiomyocytes. Cytosolic levels of HSPB5 in the LV myocardium were similar between groups (Figure Oral GGA treatment redistributes HSPB5 and HSPB1 from the cytosol to the myofilaments in the left ventricle of obese ZSF1 rats. (a and b) HSPB5 and HSPB1 levels were similar between myocardia of all groups in cytosolic fraction. (c and d) myofilament levels of HSPB5 and HSPB1 were higher in the myocardium of obese ZSF1 rats treated with GGA when compared to vehicle‐treated obese and lean ZSF1 rats. (e and f) There was a redistribution of HSPB5 and HSPB1 to the myofilaments (myofilament expression levels relative to cytosolic expression levels) in the GGA‐treated obese ZSF1 rats compared to lean and vehicle‐treated obese ZSF1 rats, although this was particularly strong for HSPB1. Data are expressed as mean ± SEM, Immunofluorescence staining confirmed a primarily myofilament localization of HSPB5 and HSPB1 in the myocardium of all rats (Figures 