| Autor: |
Edward J. Miller, Timothy Calamaras, Aly Elezaby, Aaron Sverdlov, Fuzhong Qin, Ivan Luptak, Ke Wang, Xinxin Sun, Andrea Vijay, Dominique Croteau, Markus Bachschmid, Richard A. Cohen, Kenneth Walsh, Wilson S. Colucci |
| Jazyk: |
angličtina |
| Rok vydání: |
2016 |
| Předmět: |
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| Zdroj: |
Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease, Vol 5, Iss 1 (2016) |
| Druh dokumentu: |
article |
| ISSN: |
2047-9980 |
| DOI: |
10.1161/JAHA.115.002277 |
| Popis: |
BackgroundMyocardial hypertrophy and dysfunction are key features of metabolic heart disease due to dietary excess. Metabolic heart disease manifests primarily as diastolic dysfunction but may progress to systolic dysfunction, although the mechanism is poorly understood. Liver kinase B1 (LKB1) is a key activator of AMP‐activated protein kinase and possibly other signaling pathways that oppose myocardial hypertrophy and failure. We hypothesized that LKB1 is essential to the heart's ability to withstand the metabolic stress of dietary excess. Methods and ResultsMice heterozygous for cardiac LKB1 were fed a control diet or a high‐fat, high‐sucrose diet for 4 months. On the control diet, cardiac LKB1 hearts had normal structure and function. After 4 months of the high‐fat, high‐sucrose diet, there was left ventricular hypertrophy and diastolic dysfunction in wild‐type mice. In cardiac LKB1 (versus wild‐type) mice, high‐fat, high‐sucrose feeding caused more hypertrophy (619 versus 553 μm2, P |
| Databáze: |
Directory of Open Access Journals |
| Externí odkaz: |
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