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Belda, E.* ; Voland, L.* ; Tremaroli, V.* ; Falony, G.* ; Adriouch, S.* ; Assmann, K.E.* ; Prifiti, E.* ; Aron-Wisnewsky, J.* ; Debédat, J.* ; Le Roy, T.* ; Nielsen, T.* ; Amouyal, C.* ; Andre, S.* ; Andreelli, F.* ; Blüher, M.* ; Chakaroun, R.* ; Chilloux, J.* ; Coelho, L.P.* ; Dao, M.C.* ; Das, P.* ; Fellahi, S.* ; Forslund, S.K.* ; Galleron, N.* ; Hansen, T.H.* ; Holmes, B.* ; Ji, B.* ; Krogh Pedersen, H.* ; Le, P.* ; Le Chatelier, E.* ; Lewinter, C.* ; Mannerås-Holm, L.* ; Marquet, F.* ; Myridakis, A.* ; Pelloux, V.* ; Pons, N.* ; Quinquis, B.* ; Rouault, C.* ; Roume, H.* ; Salem, J.E.* ; Sokolovska, N.* ; Søndertoft, N.B.* ; Touch, S.* ; Vieira-Silva, S.* ; Galan, P.* ; Holst, J.* ; Gøtze, J.P.* ; Køber, L.* ; Vestergaard, H.* ; Hansen, T.* ; Hercberg, S.* ; Oppert, J.M.* ; Nielsen, J.* ; Letunic, I.* ; Dumas, M.E.* ; Stumvoll, M. ; Pedersen, O.B.* ; Bork, P.* ; Ehrlich, S.D.* ; Zucker, J.D.* ; Bäckhed, F.* ; Raes, J.* ; Clément, K.*

Impairment of gut microbial biotin metabolism and host biotin status in severe obesity: Effect of biotin and prebiotic supplementation on improved metabolism.

Gut 71, 2463-2480 (2022)
Postprint Forschungsdaten DOI PMC
Open Access Hybrid
Creative Commons Lizenzvertrag
OBJECTIVES: Gut microbiota is a key component in obesity and type 2 diabetes, yet mechanisms and metabolites central to this interaction remain unclear. We examined the human gut microbiome's functional composition in healthy metabolic state and the most severe states of obesity and type 2 diabetes within the MetaCardis cohort. We focused on the role of B vitamins and B7/B8 biotin for regulation of host metabolic state, as these vitamins influence both microbial function and host metabolism and inflammation. DESIGN: We performed metagenomic analyses in 1545 subjects from the MetaCardis cohorts and different murine experiments, including germ-free and antibiotic treated animals, faecal microbiota transfer, bariatric surgery and supplementation with biotin and prebiotics in mice. RESULTS: Severe obesity is associated with an absolute deficiency in bacterial biotin producers and transporters, whose abundances correlate with host metabolic and inflammatory phenotypes. We found suboptimal circulating biotin levels in severe obesity and altered expression of biotin-associated genes in human adipose tissue. In mice, the absence or depletion of gut microbiota by antibiotics confirmed the microbial contribution to host biotin levels. Bariatric surgery, which improves metabolism and inflammation, associates with increased bacterial biotin producers and improved host systemic biotin in humans and mice. Finally, supplementing high-fat diet-fed mice with fructo-oligosaccharides and biotin improves not only the microbiome diversity, but also the potential of bacterial production of biotin and B vitamins, while limiting weight gain and glycaemic deterioration. CONCLUSION: Strategies combining biotin and prebiotic supplementation could help prevent the deterioration of metabolic states in severe obesity. TRIAL REGISTRATION NUMBER: NCT02059538.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Diabetes Mellitus ; Intestinal Bacteria ; Micronutrients ; Nutrition ; Obesity; Chromium Picolinate; Expression; Diet; Overweight; Health
Sprache englisch
Veröffentlichungsjahr 2022
HGF-Berichtsjahr 2022
ISSN (print) / ISBN 0017-5749
e-ISSN 1468-3288
Zeitschrift Gut (eGut)
Quellenangaben Band: 71, Heft: 12, Seiten: 2463-2480 Artikelnummer: , Supplement: ,
Verlag BMJ Publishing Group
Verlagsort British Med Assoc House, Tavistock Square, London Wc1h 9jr, England
Begutachtungsstatus Peer reviewed
Institut(e) Helmholtz Institute for Metabolism, Obesity and Vascular Research (HI-MAG)
POF Topic(s) 30201 - Metabolic Health
Forschungsfeld(er) Helmholtz Diabetes Center
PSP-Element(e) G-506500-001
Förderungen JPI-Microdiet study
French Agency of Research (ANR-CAPTOR, ANR-DeepIntegromics)
Fondation pour la Recherche Medicale
Deutsche Forschungsgemeinschaft (DFG)
LeDucq Foundation
European Union
DOI 10.1136/gutjnl-2021-325753
WOS ID WOS:000742089300001
PubMed ID 35017197
Erfassungsdatum 2022-02-08
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