AI Article Synopsis
- This study investigates how tributyrin (TB) affects the growth of juvenile grass carp and its influence on the PepT1 gene related to nutrient absorption in their intestines.
- Experimentation through feeding trials, cell trials, and injection trials showed that the right amounts of TB (0.5 g/kg and 1.0 g/kg) significantly enhance the growth of the fish and boost the expression of specific intestinal genes involved in oligopeptide transport.
- The findings suggest that TB regulates the PepT1 gene through a pathway involving the genes CDX2 and SP1, which could improve our understanding of how dietary TB influences fish growth and nutrient uptake.
Article Abstract
The nutritional functions of tributyrin (TB) have been extensively studied, but questions remain regarding its influence on the growth of juvenile grass carp () 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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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9558947 | PMC |
| http://dx.doi.org/10.3390/ani12192498 | DOI Listing |
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