B12 promotes gut dysbiosis and an inflammatory microenvironment that potentiates <i>Tet2</i>-deficient hematopoiesis.

ABSTRACT: Recent studies have linked elevated vitamin B12 serum levels with the presence of clonal hematopoiesis (CH) and an increased risk of developing myeloid malignancy. High B12 supplementation increases serum levels, alters gut microbial composition, and reduces the production of short-chain fatty acids (SCFAs), which help maintain gut barrier function and mucosal integrity. TET2 mutation is a frequent driver of CH that progresses in a positive feedback loop in response to microbial signals suggesting that B12 may influence CH via the gut microbiome. We evaluated the microenvironmental effects of B12 supplementation in a Tet2-deficient model of CH and found that B12 enhances myelopoiesis, heightens the responses of myeloid cells to bacterial stimuli, and increases the levels of c

SUBMITTER: Lyon PD 

PROVIDER: S-EPMC12407742 | biostudies-literature | 2025 Aug

REPOSITORIES: biostudies-literature