The amount of energy available to a cell is controlled by the protein AMPK, which senses when a cell has low levels of energy and triggers the cell to generate more. Mutations in one of the AMPK subunits (gamma-2) leading to increased AMPK activity are associated with heart failure characterized by the accumulation of high levels of the energy source glycogen in heart muscle cells.
However, the mechanisms by which these mutations lead to heart failure have not been defined.
In a study that appears online on April 12 in advance of publication in the May print issue of the Journal of Clinical Investigation, Rong Tian and colleagues from Brigham and Women's Hospital, Boston, used mice expressing one of the mutant forms of the gamma-2 AMPK subunit in heart muscle cells to show that increased AMPK activity is associated with altered metabolism in the heart muscle cells.
The cells were found to take up an increased amount of glucose and to store this as glycogen, leading to increased amounts of glycogen in the heart muscle cells. This effect of AMPK is of clinical relevance since it suggests that activation of AMPK, which is being considered as a potential treatment for type 2 diabetes, might lead to heart failure.
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