Jenkins, B., Seyssel, K., Chiu, S. et al. Odd Chain Fatty Acids; New Insights of the Relationship Between the Gut Microbiota, Dietary Intake, Biosynthesis and Glucose Intolerance. Sci Rep 7, 44845 (2017). https://doi.org/10.1038/srep44845
Odd chain fatty acids : new insights of the relationship between the gut microbiota, dietary intake, biosynthesis and glucose intolerance
|Author:||Jenkins, Benjamin J.1; Seyssel, Kevin2,3; Chiu, Sally4;|
1Univ Cambridge, Med Res Council Human Nutr Res, Elsie Widdowson Lab, Fulbourn Rd, Cambridge CB1 9NL, England.
2Lyon Univ, INSERM, CarMeN Lab, U1060, F-69310 Pierre Benite, France.
3Univ Lyon 1, Ctr Hosp Lyon Sud, CRNH Rhone Alpes, CENS, F-69310 Pierre Benite, France.
4Childrens Hosp, Oakland Res Inst, 5700 Martin Luther King Jr Way, Oakland, CA 94609 USA.
5Tungs Taichung MetroHarbor Hosp, Dept Pediat, Taichung 435, Taiwan.
6Taichung Vet Gen Hosp, Ctr Geriatr & Gerontol, Div Endocrinol & Metab, 1650 Sec 4,Taiwan Blvd, Taichung 407, Taiwan.
7Univ Hohenheim, Inst Food Chem, Garbenstr 28, D-70599 Stuttgart, Germany.
8Univ Oulu, Bioctr Oulu, Fac Biochem & Mol Med, POB 5400, FI-90014 Oulu, Finland.
9Univ Paris Saclay, UMR CEA INRA Serv Pharmacol & Immunoanal, Lab Immuno Allergie Alimentaire, F-91991 Gif Sur Yvette, France.
10Czech Acad Sci, Inst Microbiol, Lab Gnotobiol, Prague 54922, Czech Republic.
11Taichung Vet Gen Hosp, Dept Med Res, 1650 Sec 4,Taiwan Blvd, Taichung 407, Taiwan.
12Vanderbilt Univ, Sch Med, Dept Mol Physiol & Biophys, 702 Light Hall, Nashville, TN 37232 USA.
13Katholieke Univ Leuven, Lab Lipid Biochem & Prot Interact LIPIT, Campus Gasthuisberg,Herestr Box 601, B-3000 Louvain, Belgium.
14Louisiana State Univ, Coll Med, Hlth Sci Ctr, Dept Pharmacol & Expt Therapeut, 1901 Perdido Str, New Orleans, LA 70112 USA.
15Univ Cambridge, Cambridge Univ Hosp, NIHR BRC Core Metabol & Lipid Lab, Level 4,Lab Block, Cambridge, England.
|Online Access:||PDF Full Text (PDF, 0.5 MB)|
|Persistent link:|| http://urn.fi/urn:nbn:fi-fe202103258449
|Publish Date:|| 2021-03-25
Recent findings have shown an inverse association between circulating C15:0/C17:0 fatty acids with disease risk, therefore, their origin needs to be determined to understanding their role in these pathologies. Through combinations of both animal and human intervention studies, we comprehensively investigated all possible contributions of these fatty acids from the gut-microbiota, the diet, and novel endogenous biosynthesis. Investigations included an intestinal germ-free study and a C15:0/C17:0 diet dose response study. Endogenous production was assessed through: a stearic acid infusion, phytol supplementation, and a Hacl1−/− mouse model. Two human dietary intervention studies were used to translate the results. Finally, a study comparing baseline C15:0/C17:0 with the prognosis of glucose intolerance. We found that circulating C15:0/C17:0 levels were not influenced by the gut-microbiota. The dose response study showed C15:0 had a linear response, however C17:0 was not directly correlated. The phytol supplementation only decreased C17:0. Stearic acid infusion only increased C17:0. Hacl1−/− only decreased C17:0. The glucose intolerance study showed only C17:0 correlated with prognosis. To summarise, circulating C15:0 and C17:0 are independently derived; C15:0 correlates directly with dietary intake, while C17:0 is substantially biosynthesized, therefore, they are not homologous in the aetiology of metabolic disease. Our findings emphasize the importance of the biosynthesis of C17:0 and recognizing its link with metabolic disease.
|Type of Publication:||
A1 Journal article – refereed
|Field of Science:||
The authors are grateful to the Medical Research Council for core funding (Lipid Profiling and Signalling programme grant; number UD99999906, Cambridge Lipidomics Biomarker Research Initiative; grant G0800783, MRC Human Nutrition Research PhD programme). Grant GAČR: GA15–09518S and grant Czech Science Foundation GACR: 16-06326S funded part of the gut microbiota investigation. The authors would like to acknowledge the USDA (ACNC-USDA-CRIS 6251-51000-005-03S) for funding of the dose response animal study within this manuscript. The Human study “Dairy Fat supplementation” was supported by research grants from the Hospices Civils de Lyon (Actions Incitatives); from the Programme Hospitalier de Recherche Clinique Interregional; from the Agence Nationale de la Recherche (Programme de Recherche en Nutrition Humaine and the Programme National de Recherche en Alimentation); and from the Innovation Stratégique Industrielle program of the Agence pour l’Innovation OSEO (Innovation Thérapeutique – Diabète project). K. Seyssel and M. Alligier were recipients of a doctoral fellowship from the Ministère de l’Enseignement Supérieur et de la Recherche (France). The phytol supplementation animal study was supported by grants from the Academy of Finland (138690), the Sigrid Juselius Foundation and NordForsk under the Nordic Centres of Excellence Programme in Food, Nutrition and Health, project “Mitohealth” (070010). The NIH Grant R01-DK-18243 for funding of the canine study. HACL1 knockout mouse model was supported by grants from the Flemish “Fonds Wetenschappelijk Onderzoek” (G.0721.10N) and KU Leuven (OT/14/100).
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