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Deficiency of essential dietary n-3 PUFA disrupts the caecal microbiome and metabolome in mice
Robertson, Ruairi C.; Seira Oriach, Clara; Murphy, Kiera; Moloney, Gerard M.; Cryan, John F.; Dinan, Timothy G.; Ross, R. Paul; Stanton, Catherine
Date:
2017-11-27
Copyright:
© The Authors 2017
Full text restriction information:
Access to this article is restricted until 12 months after publication by the request of the publisher
Restriction lift date:
2018-11-27
Citation:
Robertson, R. C., Seira Oriach, C., Murphy, K., Moloney, G. M., Cryan, J. F., Dinan, T. G., Ross, R. P. and Stanton, C. (2017) 'Deficiency of essential dietary n-3 PUFA disrupts the caecal microbiome and metabolome in mice', British Journal of Nutrition, 118(11), pp. 959-970. doi: 10.1017/S0007114517002999
Abstract:
n-3 PUFA are lipids that play crucial roles in immune-regulation, cardio-protection and neurodevelopment. However, little is known about the role that these essential dietary fats play in modulating caecal microbiota composition and the subsequent production of functional metabolites. To investigate this, female C57BL/6 mice were assigned to one of three diets (control (CON), n-3 supplemented (n3+) or n-3 deficient (n3−)) during gestation, following which their male offspring were continued on the same diets for 12 weeks. Caecal content of mothers and offspring were collected for 16S sequencing and metabolic phenotyping. n3− male offspring displayed significantly less % fat mass than n3+ and CON. n-3 Status also induced a number of changes to gut microbiota composition such that n3− offspring had greater abundance of Tenericutes, Anaeroplasma and Coriobacteriaceae. Metabolomics analysis revealed an increase in caecal metabolites involved in energy metabolism in n3+ including α-ketoglutaric acid, malic acid and fumaric acid. n3− animals displayed significantly reduced acetate, butyrate and total caecal SCFA production. These results demonstrate that dietary n-3 PUFA regulate gut microbiota homoeostasis whereby n-3 deficiency may induce a state of disturbance. Further studies are warranted to examine whether these microbial and metabolic disturbances are causally related to changes in metabolic health outcomes.
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