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首页> 外文期刊>The British Journal of Nutrition >Dietary L-arginine supplementation improves the intestinal development through increasing mucosal Akt and mammalian target of rapamycin signals in intra-uterine growth retarded piglets.
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Dietary L-arginine supplementation improves the intestinal development through increasing mucosal Akt and mammalian target of rapamycin signals in intra-uterine growth retarded piglets.

机译：日粮L-精氨酸补充剂可通过增加子宫内发育迟缓仔猪的粘膜Akt和雷帕霉素信号的哺乳动物靶点来改善肠道发育。

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摘要

Intra-uterine growth retardation (IUGR) impairs postnatal growth and development of the small intestine (SI) in neonatal pigs and infants. L-Arginine (Arg), a critical amino acid involved in promoting growth and metabolism in young mammals, is more deficient in IUGR fetuses. However, little is known whether dietary Arg supplementation would accelerate the impaired development of the SI induced by IUGR in piglets. In the present study, a total of six litters of newborn piglets were used. In each litter, one normal and two IUGR littermates were obtained. Piglets were fed milk-based diets supplemented with 0 (Normal), 0 (IUGR) and 0.60% Arg (IUGR+Arg) from 7 to 14 d of age, respectively. Compared with Normal piglets at 14 d of age, IUGR decreased (P<0.05) the growth performance, entire SI weight, and villus height in the jejunum and ileum. IUGR piglets had lower (P<0.05) mucosal concentrations of Arg, insulin, insulin growth factor 1, as well as phosphorylated Akt, mammalian target of rapamycin (mTOR) and p70 S6 kinase but higher (P<0.05) enterocyte apoptosis index (AI). After Arg treatment in IUGR piglets, the growth performance, weight of entire SI and mucosa, and villus height in the jejunum and ileum were increased (P<0.05). Diet supplemented with Arg also increased (P<0.05) the levels of Arg, insulin, phosphorylated Akt and mTOR in SI mucosa of IUGR piglets, and decreased (P<0.05) the AI and caspase-3 activity. In conclusion, Arg has a beneficiary effect in improving the impaired SI development in IUGR piglets via regulating cell apoptosis and activating Akt and mTOR signals in SI mucosa.
机译：宫内生长迟缓（IUGR）损害新生猪和婴儿的出生后生长和小肠（SI）的发育。 L-精氨酸（Arg）是一种参与促进年轻哺乳动物的生长和代谢的重要氨基酸，其IUGR胎儿更为缺乏。然而，鲜为人知的是，饮食中添加精氨酸是否会加速由IUGR诱导的仔猪SI受损的发展。在本研究中，总共使用了六窝新生仔猪。在每个垫料中，获得一个正常的和两个IUGR的同窝仔。仔猪分别在7至14 d的年龄接受以牛奶为基础的日粮，分别添加0（正常），0（IUGR）和0.60％Arg（IUGR + Arg）。与14d龄的正常仔猪相比，IUGR降低了空肠和回肠的生长性能，整个SI重量以及绒毛高度（P <0.05）。 IUGR仔猪的粘膜浓度较低（P <0.05）的Arg，胰岛素，胰岛素生长因子1以及磷酸化的Akt，雷帕霉素（mTOR）和p70 S6激酶的哺乳动物靶标，但肠细胞凋亡指数（AI）较高（P <0.05） ）。 IUGR仔猪经过Arg处理后，其生长性能，整个SI和粘膜的重量以及空肠和回肠的绒毛高度均增加了（P <0.05）。补充精氨酸的日粮还增加（P <0.05）IUGR仔猪SI粘膜中精氨酸，胰岛素，磷酸化的Akt和mTOR的水平，降低AI和caspase-3活性（P <0.05）。总之，Arg通过调节细胞凋亡并激活SI黏膜中的Akt和mTOR信号，在改善IUGR仔猪SI发育受损中具有有益作用。

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