Effect of Tributyrin on Growth Performance and Pathway by which Tributyrin Regulates Oligopeptide Transporter 1 in Juvenile Grass Carp (Ctenopharyngodon idellus).
Effect of Tributyrin on Growth Performance and Pathway by which Tributyrin Regulates Oligopeptide Transporter 1 in Juvenile Grass Carp (Ctenopharyngodon idellus).
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三丁酸甘油酯对草鱼幼鱼生长性能的影响及调节寡肽转运蛋白1的途径
DOI：
10.3390/ani12192498
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发表时间：
2022-09-20
期刊：
影响因子：
--
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中科院分区：
文献类型：
--
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寡肽转运蛋白1（PepT 1）在寡肽的转运和吸收中起作用，是蛋白质营养的重要组成部分，影响动物的生长。三丁酸甘油酯（TB）是丁酸的前体，在肠道营养吸收中具有与丁酸类似的功能。分析TB对草鱼生长的影响及其对PepT 1的调控途径，有助于我们更好地了解TB的功能以及通过PepT 1转运寡肽的功能，并通过饲料对其进行调控。本研究表明，饲料中添加适量的三丁酸甘油酯可促进草鱼幼鱼的生长，并提高草鱼肠道和原代肠细胞中尾型同源框2（CDX 2）、特异性蛋白1（SP1）和PepT 1的表达。此外，研究了CDX 2和SP1对PepT 1表达的调节。最后，阐明了CDX 2/SP1介导的三丁酸甘油酯对PepT 1的调节。本研究验证了三丁酸甘油酯对草鱼幼鱼生长的影响，并阐明了三丁酸甘油酯对CDX 2/SP1-PepT 1的调控途径。三丁酸甘油酯（TB）的营养功能已得到广泛研究，但其对草鱼幼鱼生长的影响及草鱼肠道PepT 1的调控途径仍存在疑问。为了回答剩下的问题，在本研究中进行了饲养试验、细胞试验和腹膜注射试验。结果表明，饲料中添加适量TB（0.5 g/kg和1.0 g/kg）可显著促进草鱼幼鱼的生长性能。与寡肽转运相关的肠基因（CDX 2、SP1和PepT 1）的表达分别在0.5g/kg TB组的饲养试验和5 mM和10 mM TB组的肠细胞试验中增加。随后，抑制剂CDX 2和SP1的注射试验表明，CDX 2或SP1的抑制降低PepT 1的mRNA表达。最后，TB和抑制剂单独或联合治疗的结果表明，CDX 2/SP1介导TB对PepT 1的调节。这些结果有助于我们更好地了解TB对草鱼幼鱼生长和PepT 1寡肽转运的影响，TB可能通过CDX 2/SP1-PepT 1途径调节这一作用。
Oligopeptide transporter 1 (PepT1) plays a role in the transportation and absorption of oligopeptides, which is an important part of protein nutrition and affects the growth of animals. Tributyrin (TB), the precursor of butyrate, exhibits similar functions to those of the butyrate in intestinal nutrients absorption. The analysis of TB on the growth of grass carp and its regulation pathway on PepT1 may help us to better understand the functions of TB and oligopeptide transportation via PepT1, which can be modulated by diet. In this study, we demonstrated that an appropriate level of tributyrin supplementation in the diet promoted the growth of juvenile grass carp and elevated the expressions of caudal type homeobox 2 (CDX2), specificity protein 1 (SP1), and PepT1 in the grass carp intestine and primary intestine cell. In addition, CDX2 and SP1 regulating the expression of PepT1 was investigated. Finally, CDX2/SP1-mediating tributyrin regulation on PepT1 was elucidated. This study verified the effect of tributyrin on the growth of juvenile grass carp and clarified the tributyrin regulation pathway on CDX2/SP1-PepT1. The nutritional functions of tributyrin (TB) have been extensively studied, but questions remain regarding its influence on the growth of juvenile grass carp (Ctenopharyngodon idellus) and the regulation pathway to PepT1 in the intestine of grass carp. To answer the remaining questions, feeding trials, cell trials, and peritoneal injection trials were conducted in this study. The results showed that an appropriate level of TB (0.5 g/kg and 1.0 g/kg) supplementation in feed significantly promoted the growth performance of juvenile grass carp. The expressions of intestine genes (CDX2, SP1 and PepT1) related to oligopeptide transportation increased in the 0.5 g/kg TB group of feeding trials and both the 5 mM and 10 mM TB groups of the intestine cell trials, respectively. Subsequently, the injection trials of inhibitors CDX2 and SP1 demonstrated that the inhibition of CDX2 or SP1 decreased the mRNA expression of PepT1. Finally, the results of independent or combined treatments of TB and the inhibitors suggested that CDX2/SP1 mediated TB regulation on PepT1. These findings may help us to better understand the functions of TB on growth and PepT1 oligopeptide transportation, which could be modulated by dietary TB through the CDX2/SP1-PepT1 pathway in juvenile grass carp.
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影响因子：
3.7
作者：
Dalmasso G;Nguyen HT;Yan Y;Charrier-Hisamuddin L;Sitaraman SV;Merlin D
通讯作者：
Merlin D
DOI：
10.3390/ani11123425
发表时间：
2021-12-01
期刊：
Animals : an open access journal from MDPI
影响因子：
--
作者：
Gong L;Xiao G;Zheng L;Yan X;Qi Q;Zhu C;Feng X;Huang W;Zhang H
通讯作者：
Zhang H
DOI：
10.3390/ani12101309
发表时间：
2022-05-20
期刊：
Animals : an open access journal from MDPI
影响因子：
--
作者：
通讯作者：
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影响因子：
4.2
作者：
Gaschott, T;Steinhilber, D;Stein, J
通讯作者：
Stein, J
影响因子：
4.5
作者：
Huang, Dongyu;Liang, Hualiang;Maulu, Sahya
通讯作者：
Maulu, Sahya