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Supplement of High Protein-Enriched Diet Modulates the Diversity of Gut Microbiota in WT or PD-1H-Depleted Mice

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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 Deinococcus were specifically enriched in pupae-fed KO mice. Bacteroidetes, Firmicutes and Akkermansia were associated with weight loss in the pupaefed group while Lachnospiraceae and Anaerobiospirillum 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.

Abstract

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 Deinococcus were specifically enriched in pupae-fed KO mice. Bacteroidetes, Firmicutes and Akkermansia were associated with weight loss in the pupaefed group while Lachnospiraceae and Anaerobiospirillum 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.

참고문헌 (36)

  1. Rock CL, "Weight loss, glycemic control, and cardiovascular disease risk factors in response to differential diet composition in a weight loss program in type 2 diabetes : a randomized controlled trial", Diabetes Care, 37, pp.1573~1580 (2014)
  2. Sargrad KR, "Effect of high protein vs high carbohydrate intake on insulin sensitivity, body weight, hemoglobin a1c, and blood pressure in patients with type 2 diabetes mellitus", J. Am. Diet Assoc, 105, pp.573~580 (2005)
  3. Johnston CS, "High-protein, low-fat diets are effective for weight loss and favorably alter biomarkers in healthy adults", J. Nutr, 3, pp.586~591 (2004)
  4. Douglas PJ, "Protein, weight management, and satiety", Am. J. Clin. Nutr, 87, pp.1558~1561 (2008)
  5. Manci EA, "High protein diet attenuates histopathologic organ damage and vascular leakage in transgenic murine model of sickle cell anemia", Exp. Biol. Med, 239, pp.966~974 (2014)
  6. Gabriele M, "Diet bioactive compounds : implications for oxidative stress and inflammation in the vascular system", Endocr. Metab. Immune Disord. Drug Targets, 17, pp.264~275 (2017)
  7. Veiga-Fernandes H, "Neuro-immune interactions at barrier surfaces", Cell, 165, pp.801~811 (2016)
  8. Matarese G, "The intricate interface between immune system and metabolism", Trends Immunol, 25, pp.193~200 (2004)
  9. Besedovsky L, "Sleep and immune function", Pflugers Arch – Eur. J. Physiol, 463, pp.121~137 (2012)
  10. Marcos A, "Changes in the immune system are conditioned by nutrition", Eur. J. Clin. Nutr, 57(Suppl 1), pp.S66~69 (2003)
  11. Everard A, "Cross-talk between akkermansia muciniphila and intestinal epithelium controls diet-induced obesity", Proc. Natl. Acad. Sci. USA, 110, pp.9066~9071 (2013)
  12. Plovier H, "A purified membrane protein from akkermansia muciniphila or the pasteurized bacterium improves metabolism in obese and diabetic mice", Nat. Med, 23, pp.107~113 (2016)
  13. Wang L, "Vista, a novel mouse ig superfamily ligand that negatively regulates t cell responses", J. Exp. Med, 208, pp.577~592 (2011)
  14. Flies DB, "Coinhibitory receptor pd-1h preferentially suppresses cd4+ t cell–mediated immunity", J. Clin. Invest, 124, pp.1966~1975 (2014)
  15. Vijay-Kumar M, "Metabolic syndrome and altered gut microbiota in mice lacking toll-like receptor 5", Science, 328, pp.228~231 (2010)
  16. Zenewicz LA, "Il-22 deficiency alters colonic microbiota to be transmissible and colitogenic", J. Immunol, 190, pp.5306~5312 (2013)
  17. Kawamoto S, "The inhibitory receptor pd-1 regulates iga selection and bacterial composition in the gut", Science, 336, pp.485~489 (2012)
  18. Edgar RC, "Uparse : highly accurate otu sequences from microbial amplicon reads", Nat. Methods, 10, pp.996~998 (2013)
  19. Caporaso JG, "Qiime allows analysis of high-throughput community sequencing data", Nat. Methods, 7, pp.335~336 (2010)
  20. Bolyen E, "Reproducible, interactive, scalable and extensible microbiome data science using QIIME 2", Nat. Biotechnol, 37, pp.852~857 (2019)
  21. Caporaso JG, "PyNAST : a flexible tool for aligning sequences to a template alignment", Bioinformatics, 26, pp.266~267 (2010)
  22. Lorenza P, "Gut microbiota dysbiosis as risk and premorbid factors of IBD and IBS along the childhood-adulthood transition", Inflamm. Bowel Dis, 22, pp.487~504 (2015)
  23. Wu GD, "Linking long-term dietary patterns with gut microbial enterotypes", Science, 334, pp.105~108 (2011)
  24. Cotillard A, "Dietary intervention impact on gut microbial gene richness", Nature, 500, pp.585~588 (2013)
  25. Varma Y, "Diet rapidly and reproducibly alters the human gut microbiome", Nature, 505, pp.559~563 (2014)
  26. Lee PC, "Succinic acid production with reduced by-product formation in the fermentation of anaerobiospirillum succiniciproducens using glycerol as a carbon source", Biotechnol. Bioeng, 72, pp.41~48 (2001)
  27. Inokuchi R, "Anaerobiospirillum succiniciproducens-induced bacteremia in a healthy man", Am. J. Emerg. Med, 32, pp.812~ (2014)
  28. Jumpertz R, "Energy-balance studies reveal associations between gut microbes, caloric load, and nutrient absorption in humans", Am. J. Clin. Nutr, 94, pp.58~65 (2011)
  29. Méndez-Salazar EO, "Altered gut microbiota and compositional changes in firmicutes and proteobacteria in mexican undernourished and obese children", Front. Microbiol, 9, pp.2494~ (2018)
  30. Jianming L, "Ganoderma lucidum polysaccharide alleviating colorectal cancer by alteration of special gut bacteria and regulation of gene expression of colonic epithelial cells", J. Funct. Foods, 47, pp.127~135 (2018)
  31. Everard A, "Cross-talk between akkermansia muciniphila and intestinal epithelium controls diet-induced obesity", Proc. Nat. Acad. Sci. USA, 110, pp.9066~9071 (2013)
  32. Anhê F F, "A polyphenol-rich cranberry extract protects from dietinduced obesity, insulin resistance and intestinal inflammation in association with increased akkermansia spp. population in the gut microbiota of mice", Gut, 64, pp.872~883 (2015)
  33. Hildebrandt MA, "High-fat diet determines the composition of the murine gut microbiome independently of obesity", Gastroenterology, 137, pp.716~1724 (2009)
  34. Everard A, "Responses of gut microbiota and glucose and lipid metabolism to prebiotics in genetic obese and diet-induced leptin-resistant mice", Diabetes, 60, pp.2775~2786 (2011)
  35. Russell WR, "High-protein, reduced-carbohydrate weight-loss diets promote metabolite profiles likely to be detrimental to colonic health", Am. J. Clin. Nutr, 5, pp.1062~1072 (2011)
  36. Riccardi G, "Dietary treatment of the metabolic syndrome--the optimal diet", Br. J. Nutr, 83(S1), pp.S143~S148 (2000)

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