BACKGROUND: Type 2 @entity6 is associated with abnormal electrical conduction and @entity1164 , but the pathogenic mechanism remains unknown. This study describes electrophysiological alterations in a diet-induced pre- @entity6 @entity35 model and examines the underlying mechanism. METHODS: @entity35 were fed either high-fat diet and @entity948 water or normal chow and water for 6  weeks. The electrophysiological properties of the whole heart was analyzed by in vivo surface ECG recordings, as wells as ex vivo in Langendorff perfused hearts during baseline, @entity63 and re-perfussion. Conduction velocity was examined in isolated tissue strips. Ion channel and gap junction conductances were analyzed by patch-clamp studies in isolated cardiomyocytes. @entity82 was examined by Masson's Trichrome staining and thin-layer chromatography was used to analyze cardiac lipid content. @entity10277 ( @entity10277 ) expression and distribution was examined by western blotting and immunofluorescence respectively. RESULTS: Following 6  weeks of feeding, @entity948 -fat fed @entity35 (FFFRs) showed QRS prolongation compared to controls (16.1        0.51 (n   =   6) vs. 14.7        0.32  ms (n   =   4), p   <   0.05). Conduction velocity was slowed in FFFRs vs. controls (0.62        0.02 (n   =   13) vs. 0.79        0.06  m/s (n   =   11), p   <   0.05) and Langendorff perfused FFFR hearts were more prone to @entity2224 during reperfusion following @entity63 (p   <   0.05). The patch-clamp studies revealed no changes in @entity4024 or @entity3529 currents, cell capacitance or gap junctional coupling. @entity10277 expression was also unaltered in FFFRs, but immunofluorescence demonstrated an increased fraction of @entity10277 localized at the intercalated discs in FFFRs compared to controls (78        3.3 (n   =   5) vs. 60        4.2  % (n   =   6), p   <   0.01). No @entity82 was detected but FFFRs showed a significant increase in cardiac @entity412 content (1.93        0.19 (n   =   12) vs. 0.77        0.13  nmol/mg (n   =   12), p   <   0.0001). CONCLUSION: Six weeks on a high @entity948 -fat diet cause electrophysiological changes, which leads to QRS prolongation, decreased conduction velocity and increased arrhythmogenesis during reperfusion. These alterations are not explained by altered gap junctional coupling, @entity4024 , or @entity3529 currents, differences in cell size or @entity82 .

Diet-induced XXXX cardiac conductance and promotes arrhythmogenesis.

@entity1164 :: ('MESH:D016757', 'Disease') :: ['sudden cardiac death'] @entity82 :: ('MESH:D005355', 'Disease') :: ['fibrosis', 'Fibrosis'] @entity4024 :: ('D012964', 'Chemical') :: ['Na(+)'] @entity3529 :: ('D011188', 'Chemical') :: ['K(+)'] @entity6 :: ('MESH:D003920', 'Disease') :: ['diabetic', 'diabetes'] @entity63 :: ('MESH:D007511', 'Disease') :: ['ischemia'] @entity948 :: ('MESH:D005632', 'Chemical') :: ['fructose'] @entity10277 :: ('24392(Tax:10116)', 'Gene') :: ['Connexin43', 'Cx43'] @entity412 :: ('CHEBI:17855', 'Chemical') :: ['triglyceride'] @entity2224 :: ('MESH:D014693', 'Disease') :: ['ventricular fibrillation'] @entity35 :: ('10116', 'Species') :: ['rat', 'Sprague-Dawley rats', 'rats']
@entity6 :: (MESH:D003920,Disease) :: ['pre-diabetes slows']
