AMP does not induce torpor
AMP does not induce torpor
复制标题
DOI：
10.1152/ajpregu.00888.2006
复制
发表时间：
2007-07-01
影响因子：
2.8
通讯作者：
Gutilla, Margaret
中科院分区：
文献类型：
--
作者：
Swoap, Steven J.;Rathvon, Meaghan;Gutilla, Margaret
休眠是一种以代谢率和体温（T-b）的精心策划的降低为特征的状态，被整个动物王国的生物体用于能量储蓄。核苷酸AMP最近被认为是小鼠麻痹的主要调节剂，因为循环AMP在禁食状态下升高，并且施用AMP导致严重的体温过低。然而，我们发现AMP诱导的低温的特征和参数与禁食诱导的小鼠麻痹发作的特征和参数不同。虽然AMP给药诱导的体温降低（最低T-b 25.2 +/- 0.6 ℃）与禁食诱导的麻木深度（24.9 +/- 1.5 ℃）相似，但ADP和ATP在降低T-b方面同样有效（最低T-b：分别为24.8 +/- 0.9 ℃和24.0 +/- 0.5 ℃）。注射腺嘌呤核苷酸后，T-b下降到低温的最大速率（AMP：-0.24 +/- 0.03; ADP：-0.24 +/- 0.02; ATP：-0.25 +/- 0.03 ℃/min）明显快于禁食诱导的麻木（-0.13 +/- 0.02 ℃/min）。在AMP给药后1分钟内，心率从755 +/- 15降至268 +/- 17次/分钟（bpm），与麻痹期间观察到的情况不同（在35分钟内从646 +/- 21降至294 +/- 19 bpm）。最后，AMP的低温效应与预先给药的腺苷受体阻滞剂减弱，表明AMP对T-b的作用是通过腺苷受体介导的。这些数据表明，腺嘌呤核苷酸注射到小鼠诱导可逆的低温状态，这是无关的禁食诱导的麻木。
Torpor, a state characterized by a well-orchestrated reduction of metabolic rate and body temperature (T-b), is employed for energetic savings by organisms throughout the animal kingdom. The nucleotide AMP has recently been purported to be a primary regulator of torpor in mice, as circulating AMP is elevated in the fasted state, and administration of AMP causes severe hypothermia. However, we have found that the characteristics and parameters of the hypothermia induced by AMP were dissimilar to those of fasting-induced torpor bouts in mice. Although administration of AMP induced hypothermia (minimum T-b 25.2 +/- 0.6 degrees C) similar to the depth of fasting-induced torpor (24.9 +/- 1.5 degrees C), ADP and ATP were equally effective in lowering T-b (minimum T-b: 24.8 +/- 0.9 degrees C and 24.0 +/- 0.5 degrees C, respectively). The maximum rate of T-b fall into hypothermia was significantly faster with injection of adenine nucleotides (AMP: -0.24 +/- 0.03; ADP: -0.24 +/- 0.02; ATP: -0.25 +/- 0.03 degrees C/min) than during fasting-induced torpor (-0.13 +/- 0.02 degrees C/min). Heart rate decreased from 755 +/- 15 to 268 +/- 17 beats per minute (bpm) within 1 min of AMP administration, unlike that observed during torpor (from 646 +/- 21 to 294 +/- 19 bpm over 35 min). Finally, the hypothermic effect of AMP was blunted with preadministration of an adenosine receptor blocker, suggesting that AMP action on T-b is mediated via the adenosine receptor. These data suggest that injection of adenine nucleotides into mice induces a reversible hypothermic state that is unrelated to fasting-induced torpor.