AMP Deaminase 3 Deficiency Enhanced 5′-AMP Induction of HypometabolismReportar como inadecuado




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A hypometabolic state can be induced in mice by 5′-AMP administration. Previously we proposed that an underlying mechanism for this hypometabolism is linked to reduced erythrocyte oxygen transport function due to 5′-AMP uptake altering the cellular adenylate equilibrium. To test this hypothesis, we generated mice deficient in adenosine monophosphate deaminase 3 AMPD3, the key catabolic enzyme for 5′-AMP in erythrocytes. Mice deficient in AMPD3 maintained AMPD activities in all tissues except erythrocytes. Developmentally and morphologically, the Ampd3−-− mice were indistinguishable from their wild type siblings. The levels of ATP, ADP but not 5′-AMP in erythrocytes of Ampd3−-− mice were significantly elevated. Fasting blood glucose levels of the Ampd3−-− mice were comparable to wild type siblings. In comparison to wild type mice, the Ampd3−-− mice displayed a deeper hypometabolism with a significantly delayed average arousal time in response to 5′-AMP administration. Together, these findings demonstrate a central role of AMPD3 in the regulation of 5′-AMP mediated hypometabolism and further implicate erythrocytes in this behavioral response.



Autor: Isadora Susan Daniels, William G. O′Brien III, Vinay Nath, Zhaoyang Zhao, Cheng Chi Lee

Fuente: http://plos.srce.hr/



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