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Alpha‐1 AMP kinase knockout mice develop cardiac hypertrophy
Author(s) -
Turk James R.,
Feng Xumin,
Casati Jennifer,
Fine Deborah,
Rubin Leona J
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a128-b
Subject(s) - medicine , endocrinology , glycogen , genetically modified mouse , atrial natriuretic peptide , lipotoxicity , transgene , chemistry , knockout mouse , myocyte , protein kinase a , immunohistochemistry , muscle hypertrophy , biology , kinase , biochemistry , gene , receptor , diabetes mellitus , insulin resistance
Transgenic mice with modifications of the gamma‐2 subunit of AMPK, exhibit a hypertrophic cardiac phenotype with increased myocyte glycogen deposits. We have observed that mice in which the alpha‐1 subunit of AMP kinase (a1AMPK) gene had been knocked out (a1AMPK KO) exhibited increased cardiac dimensions and average diameter of left ventricular cardiomyocytes as compared to age‐ and gender‐matched wildtype (WT) mice (22.0 + 2.0 versus 13.8 + 0.9 microns, P < 0.05). Fractional shortening measured by echocardiography also was reduced in KO hearts (29 +/− 2) compared to WT (36 +/− 5). Immunohistochemistry demonstrated no expression of a1AMPK in cardiomyocytes of a1AMPK KO and also suggested a trend for increased percent immunoreactivity for atrial natriuretic peptide (ANP) compared to WT mice (61048.3 + 47143.3 versus 3672.7 + 4980.7). There was no difference in sections of myocardium for tingible glycogen by the periodic acid‐Schiff method, with and without diastase. However there was accumulation of oil‐red‐o‐positive lipid droplets in the myocardium of a1AMPK KO mice as compared to WT mice, suggesting that the a1AMPK KO mouse may be a potential model for cardiac lipotoxicity.