有证据表明，维生素 D 和肠道微生物群均参与结肠癌发生过程。然而，尚不清楚补充维生素 D3 对健康成人的肠道微生物组及其代谢物有何影响。我们进行了一项双盲、随机、安慰剂对照试验，以确定健康成人服用中等剂量 (4,000 IU) 维生素 D3 12 周后发生的急性和长期微生物群结构和代谢变化。我们的结果表明，与安慰剂相比，治疗组血清 25-羟基维生素 D (25(OH)D) 显着增加 (P < 0.0001)。维生素 D3 显着增加了治疗组的成分相似性 (P < 0.0001)，并丰富了双歧杆菌科的成员。我们还发现治疗组血清 25(OH)D 百分比变化与微生物稳定性之间存在显着的负相关关系 (R = -0.52，P < 0.019)。此外，补充维生素 D3 除了导致关键肠道微生物代谢关联的剧烈重组外，还导致显着的代谢变化。总之，我们表明，健康成年人中中等剂量的维生素 D3 对粪便微生物群具有独特的急性和持久影响，并提出了维生素 D 可能影响宿主-微生物群关系的新机制。发病的结直肠癌迫切需要。维生素 D、饮食和血清水平以及肠道微生物组都与结直肠癌的病因有关。通过了解维生素 D、肠道微生物组及其代谢物之间的密切关系，我们或许能够确定可进行干预的关键机制，包括炎症和代谢功能障碍。此外，维生素 D 与由肠道微生物组代谢的胆固醇相似，因此具有产生代谢物的能力，这些代谢物可以进一步研究并用于控制结直肠癌的发病率和死亡率。

Evidence indicates that both vitamin D and the gut microbiome are involved in the process of colon carcinogenesis. However, it is unclear what effects supplemental vitamin D3 has on the gut microbiome and its metabolites in healthy adults. We conducted a double-blind, randomized, placebo-controlled trial to identify the acute and long-term microbiota structural and metabolite changes that occur in response to a moderate dose (4,000 IU) of vitamin D3 for 12 weeks in healthy adults. Our results demonstrated a significant increase in serum 25-hydroxy-vitamin D (25(OH)D) in the treatment group compared to placebo (P < 0.0001). Vitamin D3 significantly increased compositional similarity (P < 0.0001) in the treatment group, and enriched members of the Bifidobacteriaceae family. We also identified a significant inverse relationship between the percent change in serum 25(OH)D and microbial stability in the treatment group (R = -0.52, P < 0.019). Furthermore, vitamin D3 supplementation resulted in notable metabolic shifts, in addition to resulting in a drastic rewiring of key gut microbial-metabolic associations. In conclusion, we show that a moderate dose of vitamin D3 among healthy adults has unique acute and persistent effects on the fecal microbiota, and suggest novel mechanisms by which vitamin D may affect the host-microbiota relationship.Preventative measures to reduce the rise in early-onset colorectal cancer are of critical need. Both vitamin D, dietary and serum levels, and the gut microbiome are implicated in the etiology of colorectal cancer. By understanding the intimate relationship between vitamin D, the gut microbiome, and its metabolites, we may be able to identify key mechanisms that can be targeted for intervention, including inflammation and metabolic dysfunction. Furthermore, the similarity of vitamin D to cholesterol, which is metabolized by the gut microbiome, gives precedence to its ability to produce metabolites that can be further studied and leveraged for controlling colorectal cancer incidence and mortality.