Relevance of Biotin Deficiency in Patients with Inflammatory Bowel Disease and Utility of Serum 3 Hydroxyisovaleryl Carnitine as a Practical Everyday Marker.
3-hydroxyisovaleryl carnitine
biotin deficiency
inflammatory bowel disease
Journal
Journal of clinical medicine
ISSN: 2077-0383
Titre abrégé: J Clin Med
Pays: Switzerland
ID NLM: 101606588
Informations de publication
Date de publication:
20 Feb 2022
20 Feb 2022
Historique:
received:
15
01
2022
revised:
13
02
2022
accepted:
15
02
2022
entrez:
25
2
2022
pubmed:
26
2
2022
medline:
26
2
2022
Statut:
epublish
Résumé
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. 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. 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. 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.
Sections du résumé
BACKGROUND
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
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
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
CONCLUSIONS
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.
Identifiants
pubmed: 35207391
pii: jcm11041118
doi: 10.3390/jcm11041118
pmc: PMC8877558
pii:
doi:
Types de publication
Journal Article
Langues
eng
Références
Am J Physiol. 1999 Oct;277(4):C605-13
pubmed: 10516089
Int J Immunopathol Pharmacol. 2009 Jan-Mar;22(1):63-71
pubmed: 19309553
World J Gastroenterol. 2016 Jan 21;22(3):933-48
pubmed: 26811638
Nat Commun. 2015 Jul 09;6:7726
pubmed: 26158509
J Nutr Biochem. 2013 Dec;24(12):2138-43
pubmed: 24183308
Nutrients. 2017 Apr 13;9(4):
pubmed: 28406440
Clin Transl Gastroenterol. 2013 Apr 18;4:e33
pubmed: 23594800
Am J Physiol Gastrointest Liver Physiol. 2016 Sep 1;311(3):G561-70
pubmed: 27492331
J Nutrigenet Nutrigenomics. 2010;3(1):18-30
pubmed: 20798549
Am J Physiol Cell Physiol. 2016 Sep 1;311(3):C386-91
pubmed: 27413170
Eur J Clin Nutr. 1989 Mar;43(3):169-73
pubmed: 2499449
Am J Clin Nutr. 1998 Mar;67(3):431-7
pubmed: 9497186
J Nutr. 2009 May;139(5):1031-6
pubmed: 19261731
Ann Nutr Metab. 2012;61(3):246-53
pubmed: 23183297
World J Gastroenterol. 2014 Jan 7;20(1):6-21
pubmed: 24415853
J Nutr. 2009 Jan;139(1):154-7
pubmed: 19056637
Can J Physiol Pharmacol. 2015 Dec;93(12):1091-6
pubmed: 26168302
Curr Opin Clin Nutr Metab Care. 2010 Nov;13(6):690-7
pubmed: 20823774
J Altern Complement Med. 2013 Aug;19(8):704-8
pubmed: 23379830
Biofactors. 2009 Jan-Feb;35(1):36-46
pubmed: 19319844
Am J Physiol Gastrointest Liver Physiol. 2013 Jan 1;304(1):G64-71
pubmed: 23104561
Am J Clin Nutr. 2004 Oct;80(4):932-5
pubmed: 15447901
Int J Vitam Nutr Res. 1988;58(4):428-35
pubmed: 3149627
Sci Rep. 2014 Apr 24;4:4768
pubmed: 24759680
J Immunol. 2018 Apr 15;200(8):2563-2570
pubmed: 29531163
Inflamm Bowel Dis. 2017 Jan;23(1):152-157
pubmed: 27930412
Scand J Gastroenterol. 2013 Nov;48(11):1272-7
pubmed: 24063425
Front Nutr. 2019 Apr 17;6:48
pubmed: 31058161
Expert Rev Gastroenterol Hepatol. 2014 Nov;8(8):909-23
pubmed: 25047396
JPEN J Parenter Enteral Nutr. 2007 Jul-Aug;31(4):311-9
pubmed: 17595441
Cell Mol Gastroenterol Hepatol. 2020;9(4):557-567
pubmed: 31786364
Inflamm Bowel Dis. 2015 Nov;21(11):2708-17
pubmed: 26348447
Adv Nutr. 2012 Mar 01;3(2):213-4
pubmed: 22516729
World J Gastroenterol. 2015 Feb 7;21(5):1614-20
pubmed: 25663781
Autoimmun Rev. 2020 Nov;19(11):102672
pubmed: 32942038
Nutr Rev. 2008 Aug;66 Suppl 1:S46-8
pubmed: 18673490
Gastroenterology. 2014 May;146(5):1278-88.e1-2
pubmed: 24503130
Front Immunol. 2016 Aug 02;7:290
pubmed: 27531998
Int J Mol Sci. 2020 Dec 31;22(1):
pubmed: 33396382
Int J Vitam Nutr Res. 1984;54(2-3):217-22
pubmed: 6500847
Expert Opin Drug Metab Toxicol. 2016;12(3):327-44
pubmed: 26699811
Nutrition. 1997 Nov-Dec;13(11-12):991-2
pubmed: 9433719
Inflamm Bowel Dis. 2014 Aug;20(8):1407-15
pubmed: 24983982
Nat Rev Gastroenterol Hepatol. 2013 Oct;10(10):585-95
pubmed: 23835489
J Crohns Colitis. 2019 Feb 1;13(2):144-164
pubmed: 30137275
Surg Clin North Am. 2011 Aug;91(4):771-85, viii
pubmed: 21787967
Expert Rev Endocrinol Metab. 2008 Nov 1;3(6):715-724
pubmed: 19727438
Am J Gastroenterol. 1989 Jul;84(7):744-8
pubmed: 2500847
Arch Biochem Biophys. 1999 Jun 1;366(1):95-106
pubmed: 10334869
Am J Clin Nutr. 2010 Dec;92(6):1399-405
pubmed: 20943794
J Crohns Colitis. 2019 Mar 26;13(3):273-284
pubmed: 30137278
Am J Physiol. 1998 Nov;275(5):C1365-71
pubmed: 9814986
J Nutr. 2009 Nov;139(11):2044-8
pubmed: 19741203
Subcell Biochem. 2012;56:1-19
pubmed: 22116691
J Nutr. 2006 Jul;136(7):1763-5
pubmed: 16772434
Acta Haematol. 2019;142(1):30-36
pubmed: 30970351
J Pediatr Gastroenterol Nutr. 2007 Nov;45(5):538-45
pubmed: 18030230
Gut. 2006 Mar;55(3):426-31
pubmed: 16474109
J Pediatr Gastroenterol Nutr. 1998 Mar;26(3):245-50
pubmed: 9523856
Dig Dis Sci. 1993 Sep;38(9):1614-8
pubmed: 8359072
Am J Gastroenterol. 2004 Nov;99(11):2178-85
pubmed: 15555000
Inflamm Bowel Dis. 2014 Jun;20(6):1120-8
pubmed: 24739632
J Leukoc Biol. 2008 Apr;83(4):912-20
pubmed: 18174365
Biochem J. 2011 Aug 1;437(3):357-72
pubmed: 21749321