Premium
The effect of vitamin B6 insufficiency in mice on inflammation caused by diet‐induced obesity.
Author(s) -
Sakakeeny Lydia Barrett,
Roubenoff Ronenn,
Bujanover Yoram,
Obin Martin,
Selhub Jacob
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.910.2
Subject(s) - inflammation , proinflammatory cytokine , cd11c , endocrinology , medicine , adipose tissue , obesity , immunology , interleukin 10 , vitamin d and neurology , immune system , biology , biochemistry , gene , phenotype
In humans, severity of inflammatory diseases (RA, IBD) and/or expression of inflammatory markers (CRP) are inversely associated with plasma vitamin B6 levels despite adequate intake. These observations suggest that the vitamin B6 deficit associated with inflammation results from increased utilization of vitamin B6 in inflammatory processes. To explore this hypothesis, we assessed the effect of reduced vitamin B6 (intake or antagonism by 4DPD) on adipose tissue (AT) inflammation in male C57BL/6 mice made obese by a high fat diet. Obesity is associated with chronic AT inflammation mediated by Th1 lymphokines (IFN‐γ, IP‐10) and by classically‐activated (M1‐polarized) CD11c+ macrophages (ATMs) that infiltrate AT and express proinflammatory mediators. Resident, M2‐polarized ATMs (CD11c‐) antagonize the pro‐inflammatory actions of infiltrating ATMs in part through production of IL‐10 . In the present study partial (50‐60%) B6 depletion was associated with reductions in IFN‐γ, IP‐10 and CD11c and coincident increases in Il‐10 gene expression in perigonadal AT of obese mice as compared with weight‐matched, B6‐replete controls. These data suggest that B6 status can regulate the Th1/Th2 and M1/M2 balance of obesity‐associated AT inflammation. Ongoing FACS will determine if and how low B6 status alters T cell and ATM populations and polarization in obesity.