Xie Yajun, Zhao Ping, Han Zhigang, Li Wei, Shi Dan, Xu Lei, Yi Qiying
The M.O.E. Key Laboratory of Laboratory Medical Diagnostics, The College of Laboratory Medicine, Chongqing Medical University, P.R. China.
State Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing, P.R. China.
J Microbiol Biotechnol. 2021 Feb 28;31(2):207-216. doi: 10.4014/jmb.2008.08003.
Supplement of high-protein food plays an important role in improving the symptoms of malnutrition and the immune capacity of the body, but the association of high-protein diet and gut microbiota remained unaddressed. Here, we systematically analyzed the internal organs and gut microbiota in C57(WT) or PD-1H-depleted (KO) mice (T cells were activated) fed with pupae or feed for six weeks. We observed that the body weight gain in the mice fed with pupae increased less significantly than that of the feed group, while the villi and small intestine lengths in the pupa group were reduced compared with that of mice given feed. However, the average body weight of the KO mice increased compared with that of the WT mice fed with pupae or feed. Pupae increased the concentration of blood glucose in WT, but not in KO mice. Moreover, in the feed group, there was no difference in the weight of the internal organs between the WT and KO mice, but in the pupae-fed group, liver weight was decreased and spleen weight was increased compared with that of KO mice. The amounts/plural/amounts of Melainabacteria, Chloroflexi, and Armatimonadetes were specifically upregulated by pupae, and this upregulation was weakened or eliminated by PD-1H depletion. Some bacteria with high abundance in the feed-fed KO mice, such as Deferribacteres, Melainabacteria, Acidobacteria, Bacteroidetes, Spirochaetes and Verrucomicrobia, were decreased in pupae-fed KO mice, and Proteobacteria and were specifically enriched in pupae-fed KO mice. Bacteroidetes, Firmicutes and were associated with weight loss in the pupaefed group while and were related glucose metabolism and energy consumption. Based on high-throughput sequencing, we discovered that some gut bacteria specifically regulated the metabolism of a high-protein diet, and PD-1H deficiency improved life quality and sustained blood glucose. Moreover, PD-1H responses to high-protein diet through modulating the type and quantity of gut bacteria. These findings provide evidence about the association among gut microbiota, T cell activation (for PD-1H depletion) and high-protein diet metabolism, have important theoretical significance for nutrition and health research.
补充高蛋白食物在改善营养不良症状和提高机体免疫能力方面发挥着重要作用，但高蛋白饮食与肠道微生物群的关联仍未得到解决。在此，我们系统地分析了用蛹或饲料喂养六周的C57（野生型，WT）或PD - 1H缺失（基因敲除，KO）小鼠（T细胞被激活）的内脏器官和肠道微生物群。我们观察到，喂食蛹的小鼠体重增加比饲料组明显更少，而蛹组的绒毛和小肠长度与喂食饲料的小鼠相比有所减少。然而，与喂食蛹或饲料的野生型小鼠相比，基因敲除小鼠的平均体重增加了。蛹增加了野生型小鼠的血糖浓度，但对基因敲除小鼠没有影响。此外，在饲料组中，野生型和基因敲除小鼠的内脏器官重量没有差异，但在喂食蛹的组中，与基因敲除小鼠相比，肝脏重量下降，脾脏重量增加。蛹特异性地上调了黑素杆菌、绿弯菌门和装甲菌门的数量，而这种上调在PD - 1H缺失时减弱或消除。在喂食饲料的基因敲除小鼠中丰度较高的一些细菌，如脱铁杆菌、黑素杆菌、酸杆菌门、拟杆菌门、螺旋体门和疣微菌门，在喂食蛹的基因敲除小鼠中减少，而变形菌门在喂食蛹的基因敲除小鼠中特异性富集。拟杆菌门、厚壁菌门与喂食蛹组的体重减轻有关，而变形菌门和放线菌门与葡萄糖代谢和能量消耗有关。基于高通量测序，我们发现一些肠道细菌特异性地调节高蛋白饮食的代谢，并且PD - 1H缺乏改善了生活质量并维持了血糖水平。此外，PD - 1H通过调节肠道细菌的类型和数量对高蛋白饮食做出反应。这些发现为肠道微生物群、T细胞激活（因PD - 1H缺失）和高蛋白饮食代谢之间的关联提供了证据，对营养与健康研究具有重要的理论意义。
