Microarray analysis of pancreatic gene expression during biotin repletion in biotin-deficient rats
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Abstract:
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 individuals with type-2 diabetes, and supplementation with biotin plus 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 by feeding them a 20% raw egg white diet for 6 weeks. Animals were then randomized into 2 groups: 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 1 week, pancreata were removed from biotin-deficient (BD) and biotin-repleted (BR) animals and RNA was isolated for microarray analysis. Biotin depletion altered gene expression in a manner 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 the results was confirmed by quantitative real-time PCR analysis, as well as by treatment of pancreatic AR42J cells with biotin. The results indicate that biotin repletion, even after lengthy deficiency, results in the rapid induction of repair processes in the pancreas.Keywords:
Biotin deficiency
Biotin deficiency
Biotinidase deficiency
Avidin
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BIOTIN deficiency in man has been extremely rare, presumably because this vitamin is ubiquitous in the diet and is also produced by the gut flora. Raw egg white contains a protein, avidin, which tightly binds biotin and renders it poorly absorbed. In 1942 Sydenstricker et al1induced biotin deficiency in adult volunteers by feeding them a diet to which 200 g of dehydrated egg white had been added. Symptoms of biotin deficiency were produced that reversed with daily injections of 75 to 300 μg of biotin. More recent reports have described infants with inborn errors in the metabolism of biotin-dependent enzymes and signs and symptoms of biotin deficiency.2,3One child with short-bowel syndrome has been described in which signs of biotin deficiency appeared in association with parenteral nutrition and antibiotic therapy, and these signs reversed with administration of 10 mg of biotin a day.4These investigators presumed this
Biotin deficiency
Avidin
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Biotin deficiency
Biotinidase deficiency
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Biotin deficiency
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To investigate the influence of intestinal flora upon the effects of biotin deficiency, we provided germ-free and conventional mice with a purified biotin-deficient diet without egg white for 20 days. Some of the biotin-deficient germ-free mice exhibited alopecia, while conventional mice on the same diet did not. Biotin levels decreased significantly in tissues of conventional and germ-free mice fed a biotin-deficient diet except in the heart of the conventional mice. Pyruvate carboxylase activity in the liver and kidney of germ-free mice fed the deficient diet also decreased significantly, while the activity in the liver of conventional mice on the same diet showed only a slight decrease. However, no significant differences in body or tissue weights were observed between germ-free and conventional mice during the short experimental period. Thus, conventional mice fed a biotin-deficient diet showed latent biotin deficiency, while germ-free animals fed the same diet exhibited severe biotin deficiency. Enteral microbial synthesis of biotin may have made some contribution to the observed amelioration of the effects of dietary biotin deficiency.
Biotin deficiency
Biotinidase deficiency
Enteral administration
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Biotin deficiency
Weanling
Calorie
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A wheat-based diet produced severe biotin deficiency symptoms appearing at the age of ten to fourteen days and becoming very severe in the third and fourth week (group 1). Biotin supplementation with 50 mug/kg (group 2) reduced the symptoms almost completely, but did not restore completely growth compared to chicks receiving the diet supplemented with 300 mug biotin/kg compared to chicks receiving the diet supplemented with 300 mug biotin/kg (group 3). The plasma level of biotin was about, or lower than, 100 ng/100 ml plasma in groups 1 and 2, indicating biotin deficiency. In group 3, plasma biotin was above 200 ng/100 ml. Liver biotin, after two weeks, was low in group 1 (less than 600 ng/g), medium in group 2 (1000 to 1500 ng/g) and in group 3 above 2000 ng/g. Plasma and liver biotin levels are found to be suitable parameters for diagnosis of subclinical biotin deficiency in chicks.
Biotin deficiency
Subclinical infection
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Biotin is a water-soluble vitamin that is classified as a B-group vitamin. In mammals, biotin serves as an essential cofactor for four carboxylases in fatty acid synthesis, branched-chain amino acid (BCAA) metabolism and gluconeogenesis. It is known that biotin deficiency causes the dysfunction of these metabolic pathways, and the resulting biochemical and physiological impairments induce skin disorders such as dermatitis, hair loss, neuritis and susceptibility to infections. Biotin deficiencies are rare in humans, as biotin is well distributed in various kinds of food. However, biotin deficiency can be induced by
Biotin deficiency
B vitamins
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Biotin-deficiency is brought about in the chick reared on a heated ration of low biotin content (O.1γ/g). This deficiency is produced in the absence of dietary egg white which is essential for the development of the avitaminosis in the rat. Deficiency symptoms are completely cured by administration of crystalline biotin methyl ester. The chick can be used in a quantitative biological assay of biotin.
Biotin deficiency
Vitamin b complex
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