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- W235981099 abstract "This study examined the effects of AMP activated kinase (AMPK) α-1 subunit inactivation (KO) on cardiac morphology and function. Mouse heart function was first assessed by ECG and echocardiography under anesthesia. Hearts were then removed, weighed, and attached to a modified Langendorff apparatus. KO mice had increased heart weight-to-body weight ratios (WT = 0.475 ± 0.006 vs KO = 0.615 ± 0.024, P<0.001). Histopathologic evaluation revealed increased myocyte diameter (P<0.05) but no change in glycogen or connective tissue content in KO mice. Northern and Western blot analysis revealed similar α- and β- myosin heavy chain content, skeletal actin isoforms, and SERCA2 content between groups. Regarding cardiac function, ECG traces were similar between groups but both fractional shortening (WT = 26.8 ± 1.1% vs KO = 33.1 ± 1.7%, P= 0.005) and ejection fraction (WT = 60.4 ± 1.7% vs KO = 69.4 ± 2.4 %, P= 0.006) were increased in KO mice. Consistent with these data, left ventricular (LV) power output was greater in KO mice (WT = 7.3 ± 2.4 vs KO = 9.5 ± 1.3 g*cm/sec, P = 0.035). Interestingly, LV power increased ~30% after epinephrine in WT hearts but was unchanged in KO hearts. In conclusion, mice lacking the AMPK α-1 subunit exhibit hypertrophy due, in large part, to enlargement of the myocyte cross sectional area. Hypertrophy was associated with increased contractility and reduced responsiveness to β-adrenergic stimulation." @default.
- W235981099 created "2016-06-24" @default.
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- W235981099 date "2009-04-01" @default.
- W235981099 modified "2023-09-23" @default.
- W235981099 title "AMP activated kinase α‐1 subunit knock‐out causes concentric hypertrophy and elevated ventricular function" @default.
- W235981099 doi "https://doi.org/10.1096/fasebj.23.1_supplement.989.4" @default.
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