Regulation of colon gene expression by vitamin B6 supplementation.

Scope: Previous studies have shown that vitamin B6 supplementation suppresses the development of colonic aberrant crypt foci (ACF), precursor lesions of colon cancer, and cell proliferation in mice receiving the colonic carcinogen, azoxymethane (AOM). This study investigated the molecular mechanism of these effects of dietary vitamin B6.

Methods And Results: To date, the mechanism by which ACFs develop is not yet fully understood.

Vitamin B6 regulates mRNA expression of peroxisome proliferator-activated receptor-γ target genes.

We previously demonstrated that vitamin B6 suppresses tumorigenesis in the colon of mice and exerts an anti-inflammatory effect through the inhibition of NF-κB activation. As these effects resemble the pharmacological properties of thiazolidinedione (TZD), a synthetic peroxisome proliferator-activated receptor-γ (PPARγ) ligand, this study was designed to examine the effect of vitamin B6 on the activation of PPARγ and adipogenesis in 3T3-L1 adipocyte cells. Pyridoxal 5'-phosphate (PLP), one of the vitamin B6 derivatives, was shown to promote adipogenesis in the 3T3-L1 adipocytes.

Vitamin B6 suppresses serine protease inhibitor 3 expression in the colon of rats and in TNF-α-stimulated HT-29 cells.

Scope: Previous reports in the areas of animal studies and, recently epidemiology, have linked anti-tumorigenic and anti-inflammatory effects to dietary vitamin B6. This study investigated the molecular mechanism of these effects of vitamin B6.

Methods And Results: DNA microarray analysis was used to obtain information on changes in colon gene expression from vitamin B6 (pyridoxine) repletion in vitamin B6-deficient rats.