Tullson P C, Rundell K W, Sabina R L, Terjung R L
Department of Physiology, State University of New York Health Science Center at Syracuse 13210, USA.
Am J Physiol. 1996 Jan;270(1 Pt 1):C76-85. doi: 10.1152/ajpcell.1996.270.1.C76.
Dietary supplementation of the creatine analogue beta-guanidinopropionic acid (beta-GPA) decreases in vitro skeletal muscle AMP deaminase (AMP-D) activity in rats. Downregulation of AMP-D activity was progressive and greater in fast-twitch muscles (70-80%) than in the slow-twitch soleus muscle (approximately 50%). The loss in AMP-D activity had little effect on inosine 5'-monophosphate accumulation in mixed-fiber muscle with intense tetanic contractions. In contrast, inosine 5'-monophosphate formation was evident earlier in fast-twitch red and white fiber sections of creatine-depleted animals during intense twitch contractions, indicating that fast-twitch muscle of beta-GPA-treated rats buffers decreases in the ATP/ADPfree ratio via deamination, even though AMP-D activity is less. Isoforms of skeletal muscle AMP-D mRNAs in mixed-fiber muscle were not altered by feeding beta-GPA for up to 9 wk. Creatine depletion did not alter total immunoreactivity; however, a redistribution of AMP-D immunoreactivity from primarily an approximately 80-kDa form toward lower apparent molecular mass species (approximately 60 and approximately 56 kDa) was observed. Posttranslational changes in AMP-D appear related to changes in activity.
在大鼠中，膳食补充肌酸类似物β-胍基丙酸（β-GPA）可降低体外骨骼肌AMP脱氨酶（AMP-D）活性。AMP-D活性的下调是渐进性的，且在快肌中（70-80%）比在慢肌比目鱼肌中（约50%）更明显。AMP-D活性的丧失对强直收缩的混合纤维肌肉中5'-单磷酸肌苷的积累影响很小。相反，在肌酸缺乏动物的快肌红肌和白肌纤维切片中，在强烈的抽搐收缩过程中，5'-单磷酸肌苷的形成更早出现，这表明β-GPA处理的大鼠的快肌通过脱氨作用缓冲了ATP/ADP游离比值的降低，尽管AMP-D活性较低。喂养β-GPA长达9周，混合纤维肌肉中骨骼肌AMP-D mRNA的同工型未发生改变。肌酸缺乏并未改变总免疫反应性；然而，观察到AMP-D免疫反应性从主要约80 kDa的形式向较低表观分子量物种（约60 kDa和约56 kDa）重新分布。AMP-D的翻译后变化似乎与活性变化有关。
