Effects of dietary biotin and avidin on growth, survival, feed conversion, biotin status and gene expression of zebrafish Danio rerio.

A study was conducted to investigate the effects of dietary avidin on growth, survival, food conversion, biotin status and gene expression of zebrafish (Danio rerio Hamilton-Buchanan) juveniles (average wet mass 0.178 g) fed 7 purified diets for 12 weeks. Experimental diets were formulated to provide 0×, 1×, 15×, 30×, 60× and 120× excess avidin versus biotin kg(-1) diet, on a molar basis; a control diet contained neither supplemental biotin nor avidin. Fish fed the control diet had the lowest percentage weight gain and the highest mortality, while the highest percentage weight gain and the lowest mortality was observed with the 0× diet (P<0.05). A linear relationship was observed between feed conversion ratio (FCR) and dietary avidin (r=0.876; P<0.0001). Fish fed diets with 120× more avidin than biotin had the highest whole-body biotin content, while the lowest value was obtained with the control and avidin-free diets (P<0.05). Elevated levels of acetyl CoA carboxylase-A (acca), methylcrotonyl CoA carboxylase (mcc) and propionyl CoA carboxylase-A (pcca) transcripts were recorded in fish fed the control diet, in comparison to the other diets. A broken-line analysis indicated that feeding zebrafish a diet with 60 times more avidin than the dietary biotin requirement level will cause biotin deficiency signs.

Biotin deficiency up-regulates TNF-alpha production in murine macrophages.

Biotin, a water-soluble vitamin of the B complex, functions as a cofactor of carboxylases that catalyze an indispensable cellular metabolism. Although significant decreases in serum biotin levels have been reported in patients with chronic inflammatory diseases, the biological roles of biotin in inflammatory responses are unclear. In this study, we investigated the effects of biotin deficiency on TNF-alpha production. Mice were fed a basal diet or a biotin-deficient diet for 8 weeks. Serum biotin levels were significantly lower in biotin-deficient mice than biotin-sufficient mice. After i.v. administration of LPS, serum TNF-alpha levels were significantly higher in biotin-deficient mice than biotin-sufficient mice. A murine macrophage-like cell line, J774.1, was cultured in a biotin-sufficient or -deficient medium for 4 weeks. Cell proliferation and biotinylation of intracellular proteins were decreased significantly in biotin-deficient cells compared with biotin-sufficient cells. Significantly higher production and mRNA expression of TNF-alpha were detected in biotin-deficient J774.1 cells than biotin-sufficient cells in response to LPS and even without LPS stimulation. Intracellular TNF-alpha expression was inhibited by actinomycin D, indicating that biotin deficiency up-regulates TNF-alpha production at the transcriptional level. However, the expression levels of TNF receptors, CD14, and TLR4/myeloid differentiation protein 2 complex were similar between biotin-sufficient and -deficient cells. No differences were detected in the activities of the NF-kappaB family or AP-1. The TNF-alpha induction by biotin deficiency was down-regulated by biotin supplementation in vitro and in vivo. These results indicate that biotin deficiency may up-regulate TNF-alpha production or that biotin excess down-regulates TNF-alpha production, suggesting that biotin status may influence inflammatory diseases.