Abstract
A variety of mammals, including several species of ground squirrels, prairie dogs, hamsters, and marsupials, innately enter into hypometabolic states, such as hibernation and daily torpor, to reduce energy expenditure during unfavorable environmental conditions such as cold winter. The mechanism of metabolic suppression in these instances is still largely unknown. Our lab has developed a method for inducing a torpor-like state in non-hibernating mammals termed Adenosine monophosphate (AMP)-Induced Deep Hypometabolism (AIDH). Using this method, we have previously shown that CD73 deficient mice (CD73KO) have a more dramatic response to AIDH when compared to WT mice. CD73 is an ecto-nucleotidase responsible for dephosphorylating AMP to Adenosine. Based on initial evidence showing AMP entering the re d blood cell (RBC), we proceeded to knock-out the main AMP degradation enzyme inside the RBCs, AMP deaminase 3 (AMPD3) in mice. In the AMPD3KO mice, we also observed an enhanced response to AIDH. To further categorize the importance of both of these enzymes, a double knock-out mouse line (DKO) deficient in both AMPD3 and CD73 were created. Here we report the initial findings of a further enhanced response to AIDH.
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