| First Author | Daniels IS | Year | 2013 |
| Journal | PLoS One | Volume | 8 |
| Issue | 9 | Pages | e75418 |
| PubMed ID | 24066180 | Mgi Jnum | J:206035 |
| Mgi Id | MGI:5547679 | Doi | 10.1371/journal.pone.0075418 |
| Citation | Daniels IS, et al. (2013) AMP deaminase 3 deficiency enhanced 5'-AMP induction of hypometabolism. PLoS One 8(9):e75418 |
| abstractText | 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. |
