Intestinal Microbial and Metabolic Profiling of Mice Fed with High Glucose and High-Fructose Diets


Increased sugar intake is implicated in Type-2 diabetes and fatty liver disease; however, the mechanisms through which glucose and fructose promote these conditions are unclear. We hypothesize that alterations in intestinal metabolite and microbiota profiles specific to each monosaccharide are involved. Two groups of six adult C57BL/6 mice were fed for 10-weeks with diets with glucose (G) or fructose (F) as sole carbohydrates, and a third group was fed with a normal chow carbohydrate mixture (N). Fecal metabolites were profiled by nuclear magnetic resonance (NMR) and microbial composition by real-time polymerase chain reaction (qPCR). Although N, G and F mice exhibited similar weight gains (with slight slower gains for F) and glucose tolerance, multivariate analysis of NMR data indicated that F mice were separated from N and G, with decreased butyrate and glutamate and increased fructose, succinate, taurine, tyrosine, and xylose. The different sugar diets also resulted in distinct intestinal microbiota profiles. That associated with fructose seemed to hold more potential to induce host metabolic disturbances compared to glucose, mainly by promoting bile acid deconjugation and taurine release and compromising intestinal barrier integrity. This may reflect the noted nonquantitative intestinal fructose absorption hence increasing its availability for microbial metabolism, a subject for further investigation.



subject category

Biochemistry & Molecular Biology


Silva, JCP; Mota, M; Martins, FO; Nogueira, C; Goncalves, T; Carneiro, T; Pinto, J; Duarte, D; Barros, AS; Jones, JG; Gil, AM

our authors


This project was developed within the scope of the project CICECO-Aveiro Institute of Materials, POCI-01-0145-FEDER-007679 (FCT ref. UID/CTM/50011/2013), financed by national funds through the FCT/MEC and when appropriate cofinanced by FEDER under the PT2020 Partnership Agreement. We also acknowledge the Portuguese National NMR Network (RNRMN), supported by FCT funds. Structural funding for the Centre for Neuroscience and Cell Biology is supported in part by FEDER European Regional Development Fund, within the PT2020 Partnership Agreement, and the COMPETE 2020 Programme within the project UID/BIA/04004/2013. This work was also funded through a Portuguese Foundation for Science and Technology (FCT) Investigator initiation grant PTDC-SAU-MET-111398-2009. J.C.P.S. and D.D. acknowledge FCT fellowship grants SFRH/BD/90259/2012 and SFRH/BD/119509/2016, respectively.

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