AMPK @entity299 results in XXXX in the absence of changes in energy metabolism.

@entity844 @entity712 @entity19 @entity1283 @entity1184 @entity1995 @entity384 @entity8582 @entity299 @entity141 @entity12440 @entity413
AIMS: @entity8582 -activated protein kinase (AMPK) is thought to be a central player in regulating myocardial metabolism and its activation has been shown to inhibit @entity1283 . Recently, @entity19 with muscle-specific deletion of AMPK b1/b2 subunits (AMPKb1b2-deficient @entity19 , b1b2M-KO) have been generated and possess <10% of normal AMPK activity in muscle. However, how/if @entity12440 alters cardiac metabolism, function, or morphology has not been investigated. Therefore, the aim of this study was to determine whether a significant loss of AMPK activity alters cardiac function, metabolism, and @entity1184 , and whether this may play a role in the pathogenesis of @entity712 . METHODS AND RESULTS: b1b2M-KO @entity19 exhibit an approximate 25% reduction in systolic and diastolic function compared with wild-type (WT) littermates. Despite the well-documented role of AMPK in controlling myocardial energy metabolism, there was no difference in basal @entity413 and @entity844 oxidation rates between b1b2M-KO and WT @entity19 . However, there was reduced AMPK-mediated phosphorylation of troponin I in @entity19 M-KO and reduced ventricular cell shortening in the presence of low @entity141 , which may explain the impaired cardiac function in these @entity19 . Interestingly, b1b2M-KO @entity19 did not display any signs of compensatory @entity1283 , which could be attributed to impaired activation of @entity1995 . CONCLUSIONS: b1b2M-KO @entity19 display evidence of @entity384 . This is the first @entity19 model of @entity12440 that demonstrates @entity299 in the absence of pathological stress and provides insights into the role of AMPK in regulating myocardial function, metabolism, @entity1184 , and the progression to @entity712 .
