Search

Background: Biotin is a water-solutions vitamin used for five mammalian carboxylases as an important coenzyme. It has a major role in fatty acids, amino acids and glucose metabolism. It is a popular dietary supplement for the treatment of fragile nails and hair loss. Objectives: The present research aimed at evaluating patients with or without biotin deficiency in telegon effluvium and determining after 3 months the impact of biotin replacement treatment. Methods: 130 patients with Telegon Efluvium (group A) and 120 healthy individuals (group B) served as a control group were studied. Methods: Those subjects who had been subjected to biotin treatment three months before the survey and reported additional hair loss reasons were eliminated. All patients were assessed for hair loss by clinical diagnosis before and after replacement treatment (hair pull test and Dermoscopic evaluation). The biotin level of serum was measured using commercially available immunosorbent assay kits. Results: Mean biotin serum levels were lower than controls between the two groups in a group. The impact of biotin replacement treatment has shown that better cases are 51.5%, improved cases are 34.6% and missing cases 13.8%. Patients with insufficient serum biotin levels were substantially improved, while non-improved cases with optimum blood biotin concentrations were significantly identified. Conclusion: Our results indicate that biotin addition had a substantial impact on hair loss, particularly in individuals with telegon effluvium who had deficiencies or inadequate biotin levels.

Thermal stress limits beef cattle production and a shorter hair coat is a key thermoregulative adaptation that allows cattle to lose heat more efficiently. The objective of this study was to identify genetic variants associated with the length of the undercoat and topcoat of cattle utilizing 1456 Brangus heifers genotyped with the Bovine GGP F250 array. Seven SNPs in the PCCA gene were significantly associated with undercoat length. PCCA belongs to the biotin transport and metabolism pathway. Biotin deficiency has been reported to cause hair loss. Four SNPs in an 110 kb including a missense mutation in the PRLR gene were significantly associated with topcoat length. Whereas the association of this polymorphism with hair length is novel, the SLICK mutation in PRLR has previously been demonstrated to significantly impact hair length in cattle. These newly detected genetic variants may contribute to a shorter hair coat and more thermotolerant animals.

Biotin is a water-soluble B-complex vitamin that functions as a cofactor of five carboxylases. Because biotin-dependent carboxylases catalyze indispensable cellular metabolic functions, biotin deficiency is considered to be involved in various pathological conditions. Moreover, biotin supplementation shows pharmacological effects in vivo. However, the precise mechanisms by which biotin deficiency induces pathological conditions remain unclear. Although abnormal metabolites are used as indicators for biotin deficiency, few comprehensive analyses of total metabolites have been reported. In this study, we analyzed the metabolomic profiles of liver extracts prepared from biotin-sufficient (BS) and -deficient (BD) mice. Thirteen of 126 metabolites showed significantly different concentrations between liver extracts from BD and BS mice. The concentrations of 5 essential amino acids, Met, Val, Thr, Ile, and Leu, and 2 conditionally essential amino acids, Cys and Tyr were significantly lower in BD mice than in BS mice. Among these, the concentrations of sulfur-containing amino acids, Cys and Met, were more than 1.5-fold lower in BD mice. The concentrations of Met metabolites, such as S-adenosylmethionine and S-adenosylhomocysteine were not significantly different between the two groups. The concentrations of glutathione and its reaction intermediates γ-Glu-Cys tendency to be lower in BD mice. The present study revealed that biotin deficiency induces an abnormal amino acids composition, especially among sulfur-containing amino acids and provide important information on the effect of biotin as a pharmacological agent.

Background & Aims Biotin is a water-soluble vitamin that is indispensable for human health. Biotin deficiency can cause failure-to-thrive, immunodeficiency, alopecia, dermatitis, and conjunctivitis. We previously reported that biotin deficiency also can lead to severe colitis in mice, which is completely reversed with supplementation. Our aim in this study was to determine if high-dose biotin supplementation can provide a therapeutic benefit in a preclinical model for inflammatory bowel disease (IBD) and to identify the molecular mechanism by which this occurs. Methods Mice were challenged with dextran sodium sulfate to induce colitis and were treated with 1 mmol/L biotin to induce or maintain remission. Clinical response was monitored by the Disease Activity Index and fecal calprotectin levels. The colon tissue was investigated for histology, length, as well as expression of inflammatory cytokines (interleukin 6, tumor necrosis factor-α, interleukin 1β), intestinal permeability, tight junctions (zonula occludens-1 and claudin-2), and the transcription factor nuclear factor-κB (NF-κB). Results Biotin therapy led to delayed onset and severity of colitis as well as accelerated healing. There was improvement in the Disease Activity Index, fecal calprotectin levels, colon length, and histology. In addition, biotin-treated mice had reduced expression of inflammatory cytokines, reduced intestinal permeability, and reduced activation of NF-κB. Conclusions Oral supplementation with biotin provides benefit for maintenance and induction of remission in the dextran sodium sulfate preclinical model for IBD. Biotin does this by reducing the activation of NF-κB, which prevents the production of inflammatory cytokines and helps maintain the integrity of the intestinal barrier. Clinically, the NF-κB pathway is important in the development of IBD and this finding suggests that biotin may have therapeutic potential for patients with IBD., Graphical abstract

Background : Biotin is a water-soluble vitamin that plays various biological roles through histone modification, such as immune functions and fetal growth. Mammalian maternal biotin deficiency during gestation induces fetal growth restriction. Preterm infants are known to be marginal biotin deficiency. However, studies on the biotin status of pregnant women under various conditions are lacking. Method : This was a retrospective case control study to analyze serum biotin concentration during pregnancy and cord blood in normal pregnancy, preterm delivery and small-for-gestational-age (SGA). Results : Twenty pregnant women with normal term delivery, 35 with preterm delivery, 24 with SGA, and 10 non-pregnant adult women were enrolled. Serum biotin concentrations of pregnant women remained low from first to third trimester. The levels of serum biotin in cord blood showed a significant positive correlation with gestational age, and that of pregnant women showed a weak positive correlation with gestational age. The maternal serum biotin levels during second and third trimester of SGA group were significantly lower than those of normal term delivery. Conclusion : This study suggests that maternal biotin deficiency during pregnancy might be the risk of preterm labor or fetal growth restriction. Further studies are required to clarify the roles of biotin in perinatal medicine. J. Med. Invest. 67 : 170-173, February, 2020.

Background: Biotin, a water-soluble B vitamin, has demonstrable anti-inflammatory properties. A biotin-deficient diet induced a colitis-like phenotype in mice, alleviable by biotin substitution. Mice with dextran sulfate sodium (DSS)-induced colitis showed biotin deficiency and diminished levels of sodium-dependent multivitamin transporter, a protein involved in biotin absorption. Biotin substitution induced remission by reducing activation of NF-κB, a transcription factor involved in intestinal permeability and inflammatory bowel disease (IBD). We investigated for the first time a possible clinical role of biotin status in IBD. Methods: In a comparative, retrospective, cross-sectional study, serum samples of 138 patients with IBD (67 female; 72 Crohn’s disease (CD), 66 ulcerative colitis (UC)) aged 18–65 years and with a mean age (±SD) of 42.5 ± 14.3 years as well as 80 healthy blood donors (40 female; 40.0 ± 10.0 years; range 20–60 years) were analyzed. Inflammation was defined as hsCRP ≥5 mg/L, and to determine biotin status, serum 3-hydroxyisovaleryl carnitine (3HIVc) levels were measured by LC-MS/MS. Results: A total of 138 patients with IBD (67f; 72CD/66 UC; 42.5 ± 14.3 years) were enrolled: 83/138 had inflammation. Mean serum 3HIVc levels were significantly higher in IBD patients but unaffected by inflammation. Biotin deficiency (95th percentile of controls: >30 nmol/L 3HIVc) was significantly more common in IBD patients versus controls. Conclusion: High serum 3HIVc levels and biotin deficiency were associated with IBD but not inflammatory activity or disease type. Our findings suggest biotin may play a role as cause or effect in IBD pathogenesis. Routine assessment and supplementation of biotin may ameliorate IBD and support intestinal integrity.

The B vitamins provide essential co-factors for central metabolism in all organisms. In plants, B vitamins have surprising emerging roles in development, stress tolerance and pathogen resistance. Hence, there is a paramount interest in understanding the regulation of vitamin biosynthesis as well as the consequences of vitamin deficiency in crop species. To facilitate genetic analysis of B vitamin biosynthesis and functions in maize, we have mined the UniformMu transposon resource to identify insertional mutations in vitamin pathway genes. A screen of 190 insertion lines for seed and seedling phenotypes identified mutations in biotin, pyridoxine and niacin biosynthetic pathways. Importantly, isolation of independent insertion alleles enabled genetic confirmation of genotype-to-phenotype associations. Because B vitamins are essential for survival, null mutations often have embryo lethal phenotypes that prevent elucidation of subtle, but physiologically important, metabolic consequences of sub-optimal (functional) vitamin status. To circumvent this barrier, we demonstrate a strategy for refined genetic manipulation of vitamin status based on construction of heterozygotes that combine strong and hypomorphic mutant alleles. Dosage analysis of pdx2 alleles in endosperm revealed that endosperm supplies pyridoxine to the developing embryo. Similarly, a hypomorphic bio1 allele enabled analysis of transcriptome and metabolome responses to incipient biotin deficiency in seedling leaves. We show that systemic pipecolic acid accumulation is an early metabolic response to sub-optimal biotin status highlighting an intriguing connection between biotin, lysine metabolism and systemic disease resistance signaling. Seed-stocks carrying insertions for vitamin pathway genes are available for free, public distribution via the Maize Genetics Cooperation Stock Center.

Biotin is a water-soluble B complex vitamin and coenzyme of five types of carboxylase and plays crucial roles in fatty acid, glucose, and amino acid metabolism. Nutritional biotin deficiency and defective enzymes essential for biotin metabolism cause inflammatory diseases such as eczema-like dermatitis and Crohn's disease; however, little is known about the pathophysiological roles of biotin. This study investigated the relationship between biotin metabolism and human allergic sensitization and diseases by measuring serum levels of biotin, total immunoglobulin E (IgE) and allergen-specific IgEs in more than 400 Japanese schoolchildren aged 6 to 12. The prevalence of allergic diseases, and environmental and life-style factors were also examined by a questionnaire. Like total IgE, serum biotin levels of children showed a log-normal distribution. Meanwhile, Spearman's rank correlation analysis showed weak but significant positive associations between serum biotin levels and total IgE (rho=0.147, p=0.0029) as well as allergen-specific IgEs against egg whites (rho=0.215, p=0.00013), cedar pollen (rho=0.176, p=0.00036), and cat dander (rho=0.130, p=0.0085). Furthermore, mean serum biotin levels in children with cedar pollinosis, but not with other allergic diseases such as asthma and allergic rhinitis, were significantly higher than in those without (p=0.0015). These results suggest a correlation between serum biotin levels and the development of cedar pollinosis. Further prospective studies are needed to evaluate the causal relationship between biotin metabolism and cedar pollen sensitization and pollinosis development.

Aim: Severe biotin deficiency associated with biotinidase enzyme deficiency in newborns is seen as severe neurological problems and hearing loss. However, the effect on the infant of deficiencies i...

Biotin is an indispensable adipogenic agent, and its ability to coordinate carbohydrate, lipid, and amino acid metabolism sensitizes insulin signaling in adipocytes. This enables the organism to adapt and survive under nutrient stress by synthesis and storage of lipids. Biotin deficiency mimics insulin resistance with alterations in cellular intermediary metabolism. Though the mechanism of lipogenesis is well established across cell types, considering its predisposition to accumulate only lipids, it is necessary to elucidate the mechanism that minimizes the effects of biotin on adipocyte protein synthesis. In order to determine the differential metabolic phenotype by biotin, the primary cultures of adipocytes were induced to differentiate in the presence and absence of excess biotin. Serum pre-incubated with avidin was used to limit biotin availability in cultured cells. Biotin restricts cellular signaling associated with protein synthesis without altering total protein content. The decline in autophagy elicits endoplasmic reticulum stress to inhibit protein synthesis by eIF2α phosphorylation possibly via accumulation of misfolded/long-lived proteins. Furthermore, the compensatory increase in Unc51 like autophagy activating kinase 1 possibly competes with eukaryotic initiation factor 4E-binding protein 1 and ribosomal p70 S6kinase phosphorylation by mechanistic targets of rapamycin complex 1 to uncouple its effect on protein synthesis. In conclusion, autophagy inhibition by biotin uncouples protein synthesis to promote lipogenesis by eliciting endoplasmic reticulum stress and differential phosphorylation of mechanistic targets of rapamycin complex 1 substrates. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1007/s12192-018-00967-9) contains supplementary material, which is available to authorized users.

Background: Leucine is an essential amino acid and a potent stimulator of muscle protein synthesis. Since muscle wasting is a major risk factor for mortality in kidney transplant recipients (KTR), dietary leucine intake might be linked to long-term mortality. Urinary 3-hydroxyisovaleryl carnitine (3-HIC) excretion, a functional marker of marginal biotin deficiency, may also serve as a marker for dietary leucine intake.Objective: In this study we aimed to investigate the cross-sectional determinants of urinary 3-HIC excretion and to prospectively investigate the association of urinary 3-HIC excretion with all-cause mortality in KTR.Design: Urinary 3-HIC excretion and plasma biotin were measured in a longitudinal cohort of 694 stable KTR. Cross-sectional and prospective analyses were performed using ordinary least squares linear regression analyses and Cox regression analyses, respectively.Results: In KTR (57% male, 53 +/- 13 years, estimated glomerular filtration rate 45 +/- 19 mL/min/1.73 m(2)), urinary 3-HIC excretion (0.80 [0.57-1.16] mu mol/24 h) was significantly associated with plasma biotin (std. beta = -0.17; P < 0.001). Subsequent adjustment for potential covariates revealed urinary creatinine excretion (std. beta = 0.24; P < 0.001) and urinary urea excretion (std. beta = 0.53; P < 0.001) as the primary determinant of urinary 3-HIC excretion. Whereas plasma biotin explained only 1% of the variance in urinary 3-HIC excretion, urinary urea excretion explained >45%. During median follow-up for 5.4 [4.8-6.1] years, 150 (22%) patients died. Log(2)-transformed urinary 3-HIC excretion was inversely associated with all-cause mortality (HR: 0.52 [0.43-0.63]; P < 0.001). This association was independent of potential confounders.Conclusions: Urinary 3-HIC excretion more strongly serves as a marker of leucine intake than of biotin status. A higher urinary 3-HIC excretion is associated with a lower risk of all-cause mortality. Future studies are warranted to explore the underlying mechanism. (C) 2020 The Authors. Published by Elsevier Ltd.

Biotin (or Vitamin B7) is a vitamin where deficiency can be caused by inadequate intake. Biotin deficiency is rare, as most people get enough biotin from diet, since many foods contain biotin. In addition to biotin from food, intestinal bacteria can synthesize biotin, which can then be absorbed by the body. Supplementation with biotin has been advocated, mainly due to proposed beneficial effects on skin, nail and hair growth. There is no evidence that high biotin intakes are toxic, but a high intake may interfere with diagnostic assays that use biotin-streptavidin technology. These tests are commonly used to measure plasma concentrations of a wide range of hormones. Erroneous results may lead to misdiagnosis of various endocrine disorders. Supplementation with high-dose biotin has been used experimental for the treatment of diseases (e.g. multiple sclerosis) and high doses are used to obtain effect on nail and hair growth. On this background a demand for tests to determine if there is a risk of obtaining false test results when using biotin-streptavidin based tests have appeared. In this paper we present a method based on column switching liquid chromatography tandem mass spectrometry for the quantification of biotin in plasma and serum and explore the effects of biotin on an immunoassay based on biotin strept(avidin) chemistry.

Mitochondrial and metabolic dysfunction are often implicated in neurological disease, but effective mechanism-based therapies remain elusive. We performed a genome-scale forward genetic screen in a Drosophila model of tauopathy, a class of neurodegenerative disorders characterized by the accumulation of the protein tau, and identified manipulation of the B-vitamin biotin as a potential therapeutic approach in tauopathy. We show that tau transgenic flies have an innate biotin deficiency due to tau-mediated relaxation of chromatin and consequent aberrant expression of multiple biotin-related genes, disrupting both carboxylase and mitochondrial function. Biotin depletion alone causes mitochondrial pathology and neurodegeneration in both flies and human neurons, implicating mitochondrial dysfunction as a mechanism in biotin deficiency. Finally, carboxylase biotin levels are reduced in mammalian tauopathies, including brains of human Alzheimer's disease patients. These results provide insight into pathogenic mechanisms of human biotin deficiency, the resulting effects on neuronal health, and a potential therapeutic pathway in the treatment of tau-mediated neurotoxicity.

Biotin is widely used in infant formula to prevent biotin deficiency of newborn babies and in beauty products as nutritional supplements for coenzymatic functions and having strong nails, shiny hair, and skin over the last few years. There is a need for the development of a fast, simple and reusable assay method to perform biotin determination at very low concentrations. Biotin determination has achieved with a prepared potentiometric biotin sensor that has a very wide concentration range (10−15 M–10−7 M) and a lower detection limit (0.3 10−15 M) with a very good regression coefficient (0.9925). A quick response (7 min), good accuracy (recovery 100.4–103.7%), reproducible, reusable (10 times), and long-term stability (3 months) have been obtained using the prepared potentiometric sensor. The obtained results have proved that the prepared potentiometric sensor can be used for biotin determination in real samples.

Background Biotin, a water-soluble B-vitamin, has been shown to have anti-inflammatory properties. A biotin-deficient diet was recently shown to induce a colitis-like phenotype in mice, alleviated by biotin substitution. Mice with DSS colitis showed biotin deficiency and significantly reduced levels of SDMT, a protein involved in biotin absorption. Oral biotin substitution reversed DSS colitis and induced remission by inhibiting NF-κB, a transcription factor that hinders inflammatory cytokine expression and plays a role in intestinal barrier integrity and IBD. We investigated for the first time a possible clinical role of biotin status in IBD. Methods In a comparative, cross-sectional study, serum samples of IBD patients were compared with samples of 80 healthy blood donors (40f;18-65y). CBC, albumin and hsCRP were determined by standard tests and samples assessed for presence/absence of inflammation (serum hsCRP, cutoff Results 138 IBD patients (67f;72 CD/66 UC;42.5±14.3y) were enrolled. Of these, 83/138 had inflammation (39f;43CD/40UC;42.5±14.6y) and 55/138 no inflammation (28f;29CD/26UC;42.5±13.9y). In IBD patients, mean serum 3HIAc levels were significantly higher vs. controls but similar with vs. without inflammation (Table 1). The reference serum 3HIAc level was calculated as 11.0–27.3 nmol/L from controls; biotin deficiency was defined as >27.3 nmol/L 3HIAc (90thPC), since no validated cut-off exists. Biotin deficiency in IBD patients was significantly greater than in controls (Table 1). Conclusion High serum 3HIAc levels were associated with IBD. In line with preclinical studies, biotin deficiency was more pronounced in IBD patients than controls. No relation was found with inflammatory activity or disease type. Our findings suggest that biotin may have a bigger role than thought in IBD; whether as a cause or effect in IBD pathogenesis warrants investigation. Routine assessment and correction of biotin status may ameliorate IBD and help maintain intestinal integrity. Table 1: 3-hydroxyisovaleryl carnitine levels and biotin deficiency

Cells obtain free energy by the catabolism of nutrients as glucose and fatty acids and use that energy to make ATP, which is used for many functions. For the generation of ATP there are several components, among them the cofactors biotin and thiamine. To obtain that energy under aerobic conditions, it is necessary to have acetyl CoA whose precursor is coenzyme A derived from pantothenic acid. In the case of biotin, it is the prosthetic group of five carboxylases that are important in the metabolism of carbohydrates, lipids, and proteins. Endogenous biotin is recycled by the action of biotinidase, which is reused by holocarboxylase synthetase. There are several genetic diseases related to biotin, among them a mutation of the sodium-dependent multivitamin transporter and multiple carboxylase deficiencies including biotinidase deficiency. Deprivation of biotin diminishes the mRNAs of liver glucokinase and increases that of phosphoenolpyruvate carboxykinase. Biotin also seems to be necessary for the normal progression of cells through the cell cycle, with deficient cells arresting in the cell cycle 1 phase. It also affects the expression of genes for carbohydrate and lipid metabolism, which is probably mediated by the activation of AMPK, the cellular energy sensor. Biotin deficiency increases insulin sensitivity by increased translocation of the transporter of glucose GLUT4.

Biotin is an essential vitamin that is covalently bound to carboxylases as coenzyme. Biotin-dependent carboxylases are a group of enzymes which are involved in a variety of cellular metabolic process, including fatty acid synthesis and gluconeogenesis; therefore, biotin deficiency may play an essential role for the metabolic abnormalities involved in inflammatory and immunological diseases. Biotin deficiency is quite rare because biotin is produced from gut microbiota in the human body and is also available from various food sources. However, some conditions, including inherited metabolic diseases, may lead to biotin deficiency. It is crucial to detect biotin deficiency as early as possible in clinical practice and recent studies have proposed screening methods for biotin deficiency. Plasma concentrations of 3-hydroxyisovaleryl carnitine, urinary excretions of 3-hydroxyisovaleric acid and 3-hydroxyisovaleryl carnitine, as well as measurement of biotinylated 3-methylcrotonyl-CoA carboxylase and propionyl-CoA carboxylase are all useful for screening for biotin deficiency.

There are three inherited biotin-responsive inherited disorders, holocarboxylase synthetase deficiency, biotinidase deficiency, and biotin–thiamine-responsive basal ganglia disease. Most importantly, the symptoms of each disorder can be improved or prevented by early detection and treatment with pharmacological doses of biotin (more than 1 mg of biotin/day). Untreated, symptomatic individuals usually develop a variety of neurological symptoms, some of which are caused by secondary biotin deficiency or the accumulation of abnormal organic acids associated with multiple carboxylase deficiency. In one of these disorders, although biotin is beneficial, its actual function is still speculative. In addition, there are two single case reports of individuals with biotin-responsive disorders due to biotin-transport defects. This chapter will discuss these biotin-responsive disorders.

Low-molecular-weight vitamin biotin is an essential nutrient substance for all animal normal growth. Previous exploration has documented that dietary biotin deficiency led to fish growth retardation and a decrease in immunity, whereas its detrimental impacts on fish other physiological status were still not revealed yet. Herein, further exploration was performed to excavate the latent influence of dietary biotin deficiency on antioxidant status, apoptosis and tight junction protein of immune organs (the skin, spleen and head kidney). In this research, grass carp (Ctenopharyngodon idella) (117.11 ± 0.48 g) as a model were fed six graded levels of biotin diets (0.012, 0.110, 0.214, 0.311, 0.427 and 0.518 mg/kg diet) in triplicate for 70 days, followed by a challenge with A. hydrophila for 6 days. Our data from above three immune organs manifested that biotin deficiency (0.012 mg/kg diet): (1) markedly increased oxidative damage degree as evidenced by the obtained highest value in all oxidative damage indicators and exhibited the lowest significant value in almost all antioxidant enzymes activities and corresponding gene expressions, where this action may be in part correlated with the modulation of Nrf2 signaling (P 0.05). Furthermore, a broken line analysis showed that dietary biotin requirement levels for on-growing grass carp is 0.245–0.354 mg/kg diet for parameters (ROS content, caspase3 and claudin-3c expression levels).

Biotin (vitamin B7) is essential for human health because of its involvement, as a cofactor, in a variety of critical cellular metabolic reactions. Previous studies have shown that biotin deficiency enhances inflammation, and certain chronic inflammatory diseases are associated with biotin deficiency; however, the mechanisms that mediate the association between biotin status and inflammation are not well understood. In this study, we examined the effect of biotin deficiency on human CD4+ T cell responses to determine their role in biotin deficiency–associated inflammation. Our investigations revealed that anti-CD3/CD28–stimulated CD4+ T cells cultured in biotin-deficient medium secreted significantly enhanced levels of the proinflammatory cytokines IFN-γ, TNF, and IL-17. Expression of the transcription factors T-bet and RORγt was increased, whereas Foxp3 expression was decreased, in biotin-deficient CD4+ T cells. The percentage of T regulatory cells was also decreased under biotin-deficient condition. A similar increase in T-bet, RORγt, and proinflammatory cytokine levels, as well as a decrease in Foxp3, was observed in inguinal lymph nodes of mice fed a biotin-deficient diet relative to pair-fed controls. Furthermore, differentiation of CD4+ T cells toward Th1 and Th17 cells was also enhanced. In vitro and in vivo investigations indicated that the increased inflammatory response was due to enhanced activation of the mammalian target of rapamycin signaling pathway in biotin-deficient CD4+ T cells. In summary, these results demonstrate that biotin deficiency enhances the inflammatory responses in CD4+ T cells, which may contribute to inflammation associated with biotin deficiency.