Microarray analysis of pancreatic gene expression during biotin repletion in biotin-deficient rats

Biotin is a B vitamin involved in multiple metabolic pathways. In humans, biotin deficiency is relatively rare but can cause dermatitis, alopecia and perosis. Low biotin levels occur in type II diabetes, and biotin supplementation with chromium may improve blood sugar control. The acute effect on pancreatic gene expression of biotin repletion following chronic deficiency is unclear, therefore we induced biotin deficiency in adult male rats via a 20% raw egg white diet for 6 weeks. Animals were then randomized: one group received a single biotin supplement and returned to normal chow lacking egg white, while the second group remained on the depletion diet. After one week, pancreata were removed from biotin-deficient (BD) and biotin-repleted (BR) animals and RNA isolated for microarray analysis. Biotin depletion altered gene expression indicative of inflammation, fibrosis and defective pancreatic function. Conversely, biotin repletion activated numerous repair and anti-inflammatory pathways reduced fibrotic gene expression and induced multiple genes involved in pancreatic endocrine and exocrine function. A subset of results was confirmed by qPCR analysis, as well as by biotin treatment of pancreatic AR42J cells. The results indicate that biotin repletion, even after lengthy deficiency, results in the rapid induction of repair processes in the pancreas.The accepted manuscript in pdf format is listed with the files at the bottom of this page. The presentation of the authors' names and (or) special characters in the title of the manuscript may differ slightly between what is listed on this page and what is listed in the pdf file of the accepted manuscript; that in the pdf file of the accepted manuscript is what was submitted by the author