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在冬眠的北极地松鼠禁食期间增加组织氮同位素比值的替代模型的检验。

A test of alternative models for increased tissue nitrogen isotope ratios during fasting in hibernating arctic ground squirrels.

机构信息

Department of Biology and Wildlife, University of Alaska Fairbanks, Fairbanks, AK 99775, USA.

出版信息

J Exp Biol. 2012 Oct 1;215(Pt 19):3354-61. doi: 10.1242/jeb.068528. Epub 2012 Jun 26.

DOI:10.1242/jeb.068528
PMID:22735347
Abstract

We describe two models explaining the increase in tissue nitrogen isotope ratios (δ(15)N) that occurs during fasting in animals. The catabolic model posits that protein breakdown selectively removes the lighter isotope of nitrogen ((14)N) from catabolized tissues, causing an increase in the proportion of heavy nitrogen isotope ((15)N). The anabolic model posits that protein synthesis during fasting results in elevated δ(15)N values, as the unreplaced loss of (14)N to urea results in a higher proportion of (15)N in plasma amino acids used for protein synthesis. We effected a range of lean mass loss in arctic ground squirrels (Urocitellus parryii) fasting during hibernation and then collected organ and muscle tissues for analysis of δ(15)N values. The catabolic model predicts increased δ(15)N values in both liver and muscle, as these tissues undergo significant catabolism during hibernation. The anabolic model predicts no change in muscle, but an increase in δ(15)N values in liver, which has high levels of protein synthesis during euthermic phases of hibernation. We found a significant increase in liver δ(15)N values and no change in muscle δ(15)N values with lean mass loss, which supports the anabolic model. Heart, small intestine and brown adipose tissue also showed an increase in δ(15)N values, indicating protein synthesis in these organ tissues during hibernation. Urine was 3.8% lighter than plasma, and both urine and plasma increased in δ(15)N values with lean mass loss. This study helps clarify the mechanisms causing δ(15)N change during nutritional stress, thus increasing its utility for physiological research and reconciling previously contradictory results.

摘要

我们描述了两种模型,用以解释动物在禁食期间组织氮同位素比值(δ¹⁵N)增加的原因。分解代谢模型认为,蛋白质分解会选择性地从分解代谢组织中去除较轻的氮同位素(¹⁴N),导致重氮同位素(¹⁵N)的比例增加。合成代谢模型则认为,禁食期间的蛋白质合成会导致 δ¹⁵N 值升高,因为尿素中¹⁴N 的无替代损失导致用于蛋白质合成的血浆氨基酸中¹⁵N 的比例升高。我们在冬眠期间禁食的北极地松鼠(Urocitellus parryii)中实现了一系列瘦体重损失,然后收集器官和肌肉组织进行 δ¹⁵N 值分析。分解代谢模型预测,肝脏和肌肉的 δ¹⁵N 值都会增加,因为这些组织在冬眠期间会经历显著的分解代谢。合成代谢模型预测肌肉的 δ¹⁵N 值不会改变,但肝脏的 δ¹⁵N 值会增加,因为肝脏在冬眠的恒温相期间有高水平的蛋白质合成。我们发现,随着瘦体重的减少,肝脏的 δ¹⁵N 值显著增加,而肌肉的 δ¹⁵N 值没有变化,这支持了合成代谢模型。心脏、小肠和棕色脂肪组织的 δ¹⁵N 值也有所增加,表明这些器官组织在冬眠期间有蛋白质合成。尿液比血浆轻 3.8%,随着瘦体重的减少,尿液和血浆的 δ¹⁵N 值都增加了。这项研究有助于阐明在营养应激期间导致 δ¹⁵N 变化的机制,从而提高其在生理研究中的应用价值,并调和先前相互矛盾的结果。

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