Dietary leucine supplementation improves intestinal health of mice through intestinal SIgA secretion

膳食亮氨酸补充通过肠道 SIgA 分泌改善小鼠肠道健康

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作者:B Song, C Zheng, C Zha, S Hu, X Yang, L Wang, H Xiao

Aims

Leucine supplementation promotes intestinal health, but the mechanism is largely unknown. This study aimed to elucidate the mechanisms underlying the beneficial effects of leucine on intestinal homeostasis.

Conclusions

Therefore, our data suggested that leucine supplementation could enhance intestinal health through the regulation of mTOR pathway and promoting SIgA secretion in the mouse intestine, which might be associated with intestinal microbiota. Significance and impact of the study: The present study found that dietary leucine supplementation of mice could improve intestinal health by enhancing intestinal SIgA secretion via a nonexclusive mechanism, which might include T cell-dependent pathway, T cell-independent pathway and gut microbiota.

Results

Female ICR mice (6-week-old) were randomly assigned into three groups: (i) mice received a basal diet; (ii) mice received a dietary 0·5% crystalline l-leucine supplementation; and (iii) mice received a dietary 1·0% crystalline l-leucine supplementation. Our results showed that leucine supplementation stimulated the secretion of SIgA in mice ileum and expression of cytokines related to SIgA production. Moreover, leucine supplementation improved the expression of mTOR and p70S6K1 expression. Further study showed that leucine supplementation markedly decreased microbiota richness and induced a shift in the Firmicutes : Bacteroidetes ratio in favour of Firmicutes. Conclusions: Therefore, our data suggested that leucine supplementation could enhance intestinal health through the regulation of mTOR pathway and promoting SIgA secretion in the mouse intestine, which might be associated with intestinal microbiota. Significance and impact of the study: The present study found that dietary leucine supplementation of mice could improve intestinal health by enhancing intestinal SIgA secretion via a nonexclusive mechanism, which might include T cell-dependent pathway, T cell-independent pathway and gut microbiota.

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