Odd Chain Fatty Acids; New Insights of the Relationship Between the Gut Microbiota, Dietary Intake, Biosynthesis and Glucose Intolerance View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2017-12

AUTHORS

Benjamin J. Jenkins, Kevin Seyssel, Sally Chiu, Pin-Ho Pan, Shih-Yi Lin, Elizabeth Stanley, Zsuzsanna Ament, James A. West, Keith Summerhill, Julian L. Griffin, Walter Vetter, Kaija J. Autio, Kalervo Hiltunen, Stéphane Hazebrouck, Renata Stepankova, Chun-Jung Chen, Maud Alligier, Martine Laville, Mary Moore, Guillaume Kraft, Alan Cherrington, Sarah King, Ronald M. Krauss, Evelyn de Schryver, Paul P. Van Veldhoven, Martin Ronis, Albert Koulman

ABSTRACT

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. More... »

PAGES

44845

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/srep44845

DOI

http://dx.doi.org/10.1038/srep44845

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1084132720

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/28332596


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