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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.

Strain-dependent differences have been used to highlight unknown genetic contributions to important behavioral and physiological end points. In this regard, the Fischer (F344) and Lewis (LEW) rat strains have often been studied because they exhibit a myriad of behavioral and physiological differences. Recently, schedule-induced polydipsia (SIP), a potential model of stress and drug abuse, has been reported to differ between the two strains (see [Pharmacol. Biochem. Behav. 67 (2002) 809]) with F344 rats displaying greater levels of consumption than LEW rats. Given the importance of SIP as a behavioral model of stress and of drug abuse, the present study further explored SIP in F344 and LEW strains by assessing the acquisition and steady-state performance of SIP (under a fixed-time 30 schedule of food delivery; FT30), its characteristic postprandial temporal licking pattern and its modulation by variations in the food delivery schedule (FT15, FT30 and FT60). F344 rats acquired SIP at a faster rate and drank at a higher asymptotic level than LEW rats. Both strains displayed the typical inverted U-shaped post-pellet pattern of drinking and changes in levels of consumption (and displacement of the initiation of post-pellet drinking) with changes in the FT value, supporting the position that the increased drinking seen in both groups was schedule induced. These strain differences in SIP are consistent with the fact that the F344 and LEW strains differ on other behavioral and physiological indices of stress and raise the issue of the use of this model in the assessment of differential drug intake between the two strains.