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餐后亮氨酸缺乏未能改变生长大鼠和成年大鼠的肌肉蛋白质合成。

Postprandial leucine deficiency failed to alter muscle protein synthesis in growing and adult rats.

作者信息

Debras Elisabeth, Prod'homme Magali, Rieu Isabelle, Balage Michèle, Dardevet Dominique, Grizard Jean

机构信息

Unité de Nutrition Humaine, UMR1019, Institut National de la Recherche Agronomique, F-63122 Saint Genès Champanelle Centre de Recherche en Nutrition Humaine d'Auvergne, Auvergne, France.

出版信息

Nutrition. 2007 Mar;23(3):267-76. doi: 10.1016/j.nut.2006.12.003.

Abstract

OBJECTIVE

This study examined the effect of a specific acute postprandial leucine deficiency on skeletal muscle protein synthesis in growing and adult rats. Because the anabolic action of dietary leucine supplementation is controversial, except during aging, we hypothesized that the maximum leucine effect might be already achieved for a normal postprandial rise of leucine. Preventing this rise during the 1- to 3-h period after feeding may reveal the leucine regulation.

METHODS

On the day of the experiment, rats were fasted (postabsorptive, PA group) or fed for 1 h a control meal (postprandial, control, PP group) or a leucine-poor meal (postprandial, PP-Leu group). Muscle protein synthesis was assessed in vivo, over the 1- to 3-h period after meal distribution, using the flooding dose method (L-1-(13)C phenylalanine).

RESULTS

As expected, the postprandial increase in plasma free leucine was specifically abolished after feeding the leucine-poor meal, whereas all the other plasma free amino acids were roughly at normal postprandial levels. Plasma insulin increased after feeding in young rats but was constant in adult rats. Plasma insulin was similar whatever dietary leucine levels. Rates of muscle protein synthesis were stimulated by feeding in gastrocnemius and soleus muscles from young rats but only in gastrocnemius muscles from adult rats. The PP-Leu group did not differ from the control PP group regarding muscle protein synthesis.

CONCLUSION

The rise in plasma free leucine is not required for the stimulation of muscle protein synthesis during the 1- to 3-h period after feeding young and adult rats, as previously observed in old rats.

摘要

目的

本研究检测了特定的急性餐后亮氨酸缺乏对生长发育期和成年大鼠骨骼肌蛋白质合成的影响。由于除衰老期间外,膳食补充亮氨酸的合成代谢作用存在争议,我们推测对于正常餐后亮氨酸的升高,可能已经达到了亮氨酸的最大效应。在进食后1至3小时内阻止这种升高可能会揭示亮氨酸的调节作用。

方法

在实验当天,大鼠禁食(吸收后状态,PA组)或进食1小时对照餐(餐后,对照,PP组)或低亮氨酸餐(餐后,PP-Leu组)。在餐后分配后的1至3小时内,使用灌注剂量法(L-1-(13)C苯丙氨酸)在体内评估肌肉蛋白质合成。

结果

正如预期的那样,喂食低亮氨酸餐后,餐后血浆游离亮氨酸的升高被特异性消除,而所有其他血浆游离氨基酸大致处于正常餐后水平。喂食后,幼鼠血浆胰岛素升高,而成年大鼠血浆胰岛素保持恒定。无论膳食亮氨酸水平如何,血浆胰岛素水平相似。喂食刺激了幼鼠腓肠肌和比目鱼肌的肌肉蛋白质合成率,但仅刺激了成年大鼠腓肠肌的肌肉蛋白质合成率。在肌肉蛋白质合成方面,PP-Leu组与对照PP组没有差异。

结论

如先前在老年大鼠中观察到的那样,喂食后1至3小时内,幼鼠和成年大鼠肌肉蛋白质合成的刺激不需要血浆游离亮氨酸升高。

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