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来自肠道微生物和饮食的维生素B12类似物对人类肠道共生丙酸产生菌有不同影响。

Vitamin B12 analogues from gut microbes and diet differentially impact commensal propionate producers of the human gut.

作者信息

Kundra Palni, Greppi Anna, Duppenthaler Monica, Plüss Serafina, Pugin Benoit, Lacroix Christophe, Geirnaert Annelies

机构信息

Laboratory of Food Biotechnology, Institute of Food, Nutrition and Health, Department of Health Sciences and Technology, Zurich, Switzerland.

出版信息

Front Nutr. 2024 Feb 8;11:1360199. doi: 10.3389/fnut.2024.1360199. eCollection 2024.

DOI:10.3389/fnut.2024.1360199
PMID:38389799
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10881866/
Abstract

To produce the health-associated metabolite propionate, gut microbes require vitamin B12 as a cofactor to convert succinate to propionate. B12 is sourced in the human gut from the unabsorbed dietary fraction and microbial production. However, experimental data for B12 production by gut microbes is scarce, especially on their produced B12-analogues. Further, the promotion of propionate production by microbially-produced and dietary B12 is not yet fully understood. Here, we demonstrated B12 production in 6 out of 8 predicted B12-producing bacteria from the human gut. Next, we showed that B12 produced by , and promoted succinate to propionate conversion of two prevalent B12-auxotrophic gut bacteria, and . Finally, we examined the propiogenic effect of commercially available B12-analogues present in the human diet (cyano-B12, adenosyl-B12 and hydroxy-B12) at two doses. The low dose resulted in partial conversion of succinate to propionate for when grown with adenosyl-B12 (14.6 ± 2.4 mM succinate and 18.7 ± 0.6 mM propionate) and hydroxy-B12 (13.0 ± 1.1 mM and 21.9 ± 1.2 mM), in comparison to cyano-B12 (0.7 ± 0.1 mM and 34.1 ± 0.1 mM). Higher doses of adenosyl-B12 and hydroxy-B12 resulted in significantly more conversion of succinate to propionate in both propionate-producing species, compared to the low dose. B12 analogues have different potential to impact the propionate metabolism of prevalent propionate producers in the gut. These results could contribute to strategies for managing gut disorders associated with decreased propionate production.

摘要

为了产生与健康相关的代谢产物丙酸,肠道微生物需要维生素B12作为辅助因子将琥珀酸转化为丙酸。人体肠道中的B12来源于未被吸收的饮食成分和微生物的产生。然而,关于肠道微生物产生B12的实验数据很少,尤其是它们产生的B12类似物。此外,微生物产生的B12和饮食中的B12对丙酸产生的促进作用尚未完全了解。在这里,我们证明了在8种预测可产生B12的人体肠道细菌中有6种能够产生B12。接下来,我们表明由[具体细菌名称1]、[具体细菌名称2]和[具体细菌名称3]产生的B12促进了两种普遍存在的B12营养缺陷型肠道细菌[具体细菌名称4]和[具体细菌名称5]的琥珀酸向丙酸的转化。最后,我们研究了人类饮食中存在的市售B12类似物(氰钴胺、腺苷钴胺和羟钴胺)在两种剂量下的促丙酸生成作用。低剂量时,当[具体细菌名称4]与腺苷钴胺(琥珀酸14.6±2.4 mM,丙酸18.7±0.6 mM)和羟钴胺(13.0±1.1 mM和21.9±1.2 mM)一起生长时,琥珀酸部分转化为丙酸,而与氰钴胺(0.7±0.1 mM和34.1±0.1 mM)相比。与低剂量相比,高剂量的腺苷钴胺和羟钴胺在两种产丙酸菌中都导致琥珀酸向丙酸的转化显著增加。B12类似物对肠道中普遍存在的产丙酸菌的丙酸代谢有不同的潜在影响。这些结果可能有助于制定与丙酸产生减少相关的肠道疾病管理策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2168/10881866/a21bdf68d8af/fnut-11-1360199-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2168/10881866/dffe310f9e58/fnut-11-1360199-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2168/10881866/666566b183cb/fnut-11-1360199-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2168/10881866/2430610dc5f1/fnut-11-1360199-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2168/10881866/609671d0c8bf/fnut-11-1360199-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2168/10881866/22f5e40fe6ef/fnut-11-1360199-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2168/10881866/a21bdf68d8af/fnut-11-1360199-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2168/10881866/dffe310f9e58/fnut-11-1360199-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2168/10881866/666566b183cb/fnut-11-1360199-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2168/10881866/2430610dc5f1/fnut-11-1360199-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2168/10881866/609671d0c8bf/fnut-11-1360199-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2168/10881866/22f5e40fe6ef/fnut-11-1360199-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2168/10881866/a21bdf68d8af/fnut-11-1360199-g006.jpg

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