scholarly journals Biotin deficiency

2019 ◽  
Author(s):  
Daniel Bell
Keyword(s):  
Biotin Deficiency

BIOTIN DEFICIENCY

The Lancet ◽  
1981 ◽  
Vol 317 (8231) ◽  
pp. 1195
Keyword(s):  
Biotin Deficiency

Sa597 DIETARY-INDUCED BIOTIN DEFICIENCY AND TAMOXIFEN-INDUCED, INTESTINE-SPECIFIC DELETION OF THE BIOTIN TRANSPORTER IN ADULT MICE LEAD TO GUT MICROBIOME PERTURBATIONS

2021 ◽  
Vol 160 (6) ◽  
pp. S-567
Author(s):  
Julianne C. Yang ◽  
Subrata Sabui ◽  
Jonathan Skupsky Jonathan P. Jacobs ◽  
Hamid M. Said
Keyword(s):  
Gut Microbiome ◽  
Biotin Deficiency ◽  
Adult Mice ◽  
Specific Deletion

scholarly journals Paradoxical Regulation of Biotin Utilization in Brain and Liver and Implications for Inherited Multiple Carboxylase Deficiency

2004 ◽  
Vol 279 (50) ◽  
pp. 52312-52318 ◽  
Author(s):  
Diana Pacheco-Alvarez ◽  
R. Sergio Solórzano-Vargas ◽  
Roy A. Gravel ◽  
Rafael Cervantes-Roldán ◽  
Antonio Velázquez ◽  
...  
Keyword(s):  
High Dose ◽  
Mrna Levels ◽  
Holocarboxylase Synthetase ◽  
Biotin Deficiency ◽  
Multiple Carboxylase Deficiency ◽  
Regulatory Impact ◽  
Normal Metabolism ◽  
Liver And Kidney ◽  
Essential Function ◽  
The Brain

Holocarboxylase synthetase (HCS) catalyzes the biotinylation of five carboxylases in human cells, and mutations of HCS cause multiple carboxylase deficiency (MCD). Although HCS also participates in the regulation of its own mRNA levels, the relevance of this mechanism to normal metabolism or to the MCD phenotype is not known. In this study, we show that mRNA levels of enzymes involved in biotin utilization, including HCS, are down-regulated during biotin deficiency in liver while remaining constitutively expressed in brain. We propose that this mechanism of regulation is aimed at sparing the essential function of biotin in the brain at the expense of organs such as liver and kidney during biotin deprivation. In MCD, it is possible that some of the manifestations of the disease may be associated with down-regulation of biotin utilization in liver because of the impaired activity of HCS and that high dose biotin therapy may in part be important to overcoming the adverse regulatory impact in such organs.

Seborrheic Dermatitis of Infants: Treatment with Biotin Injections for the Nursing Mother

PEDIATRICS ◽  
1969 ◽  
Vol 44 (6) ◽  
pp. 1014-1016
Author(s):  
Aaron Nisenson
Keyword(s):  
Breast Milk ◽  
Maternal Nutrition ◽  
Seborrheic Dermatitis ◽  
Cow’S Milk ◽  
Blood Levels ◽  
Biotin Deficiency ◽  
Nursing Mother ◽  
Limited Experience ◽  
The Relationship ◽  
Breast Fed

Four cases of extensive seborrheic dermatitis or Leiner's disease are presented which dramatically improved after the nursing mother was given injections of biotin. The relationship between seborrheic dermatitis in infants and biotin deficiency is discussed and the literature reviewed. From this review it appears that breast milk is deficient in biotin in comparison to cow's milk. The deficiency is further aggravated by poor maternal nutrition. Infection and diarrhea in the infant may also contribute to low blood levels of biotin. On the basis of this limited experience, injections of biotin to the nursing mother appear to be a useful treatment for the breast-fed infant with extensive seborrheic dermatitis.

scholarly journals Lymphocyte propionyl-CoA carboxylase and its activation by biotin are sensitive indicators of marginal biotin deficiency in humans 1–3

2006 ◽  
Vol 84 (2) ◽  
pp. 384-388 ◽  
Author(s):  
Shawna L Stratton ◽  
Anna Bogusiewicz ◽  
Matthew M Mock ◽  
Nell I Mock ◽  
Amanda M Wells ◽  
...  
Keyword(s):  
Biotin Deficiency

Biotin Deficiency in Suckling Pigs

1952 ◽  
Vol 47 (2) ◽  
pp. 203-212 ◽  
Author(s):  
W. P. Lehrer ◽  
A. C. Wiese ◽  
P. R. Moore
Keyword(s):  
Biotin Deficiency

Jurkat Cells Respond to Biotin Deficiency with Increased Nuclear Translocation of NF-kB, Mediating Cell Survival

2004 ◽  
Vol 74 (3) ◽  
pp. 209-216 ◽  
Author(s):  
Rodriguez-Melendez ◽  
Schwab ◽  
Zempleni
Keyword(s):  
Transcriptional Activation ◽  
Nuclear Translocation ◽  
Suppressor Gene ◽  
Jurkat Cells ◽  
Response To Treatment ◽  
Serum Starvation ◽  
Biotin Deficiency ◽  
Necrosis Factor Alpha ◽  
Nuclear Abundance ◽  
Nf Kappab

Members of the NF-kappaB family of transcription factors cause transcriptional activation of anti-apoptotic genes. Here we determined whether survival of biotin-deficient cells is mediated by nuclear translocation of NF-kappaB. Human T (Jurkat) cells were cultured in biotin-deficient or biotin-supplemented media; nuclear translocation of NF-kappaB was stimulated with phytohemagglutinin and phorbol-12-myristate-13-acetate. Nuclear abundance of two members (p50 and p65) of the NF-kappaB family was greater in biotin-deficient compared to biotin-supplemented cells; this effect was mediated by phosphorylation of IkappaBalpha. The nuclear enrichment of p50 and p65 in biotin-deficient cells was associated with transcriptional activation of NF-kappaB-dependent genes such as the tumor suppressor gene p53 and the anti-apoptotic gene Bfl-1/A1. Biotin-deficient cells exhibited smaller activities of the apoptotic enzyme caspase-3 in response to treatment with tumor necrosis factor alpha, and decreased cell death in response to serum starvation compared to biotin-supplemented cells. These findings suggest that NF-kappaB mediates survival of biotin-deficient cells.

The effect of biotin deficiency on the synthesis of fatty acids by yeast

1963 ◽  
Vol 70 ◽  
pp. 493-503 ◽  
Author(s):  
Heikki Suomalainen ◽  
A.J.A. Keränen
Keyword(s):  
Fatty Acids ◽  
Biotin Deficiency
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