Gut flora, otherwise knows as gut microbiota, are the bacteria that live in our digestive tract. There are roughly one thousand different species of bacteria, that are nourished partly by what we eat. Each person has their own specific gut flora and metabolism and these differ according to our dietary habits. Previous studies in mice have shown that a high-fat diet is capable of causing an imbalance in the gut flora, thus causing metabolic diseases such as diabetes or obesity.
Rémy Burcelin's research team (Inserm unit 1048, Université Toulouse III - Paul Sabatier) spent three months studying how a fatty (1) diet affected the gut flora of male mice of the same age, all with the same genetic background. Most of the mice developed diabetes while remaining thin, whereas some remained thin but did not develop diabetes. Why is this so?
In order to confirm the theory that gut flora affects the way in which our body reacts to a high-fat diet, the research team looked at the microbial profile of different types of mice (thin and diabetic and thin and non-diabetic, which indicates two phenotypes). They showed that there was a difference in the quantities of gut bacteria between diabetic and non-diabetic mice. The thin but diabetic mice presented a flora composed mainly of "bacteroidetes" type bacteria, unlike the thin and non-diabetic mice that presented a flora composed mainly of "firmicutes" type bacteria.
So is gut flora the cause or the result of metabolic disorders? To find the answer to this question, Rémy Burcelin's team directly modified the gut flora of a group of mice by adding dietary fibers and gluco-oligosaccharides to their high-fat diet. "By adding these fibers, we modulated most of the physiological characteristics. The metabolism of the mice that we treated with these fibers was similar to that of the thin, non-diabetic mice.
But the gut flora of the mice treated with fibers changed greatly compared to that of the other phenotypes observed", says Matteo Serino
Rémy Burcelin's team came to the conclusion that "the gut flora could guide the metabolism towards developing diabetes or not, depending on its profile". "Although we cannot compare the bacterial flora of a mouse with that of a human, because there is only 2% similarity, certain inflammatory mechanisms caused by certain bacteria such as Faecalibacterium prausnitzii seem to be identical". The researchers think that the bacteria present in the gut flora could be an indication as to whether or not an individual will develop diabetes. "It is possible that by adding dietary fibers that target the gut flora, we could prevent the development of metabolic diseases such as diabetes, even in persons who have a high-fat diet".
This project was partly sponsored by the "Florinflam" research program financed by the National Research Agency (ANR) and the "FLORINASH" research program financed by the seventh European Commission program. The FLORINASH project (Prevention and treatment of non-alcoholic fatty liver disease) was coordinated by Inserm under the auspices of Rémy Burcelin, Inserm research director, and was contributed to by 6 partners from 4 European countries.
(1) A diabetogenic but not obesitogenic diet.
Sources
Metabolic adaptation to a high-fat diet is associated with a change in the gut microbiota. Matteo Serino,1,2 Élodie Luche,1,2 Sandra Gres,1,2 Audrey Baylac,3 Mathieu Bergé,3 Claire Cenac,4 Aurélie Waget,1,2 Pascale Klopp,1,2 Jason Iacovoni,1,2 Christophe Klopp,5 Jérôme Mariette,5 Olivier Bouchez,6 Jerome Lluch,6 Francoise Ouarné,7 Pierre Monsan,7,8,9,10 Philippe Valet,1,2 Christine Roques,3 Jacques Amar,11 Anne Bouloumié,1,2 Vassilia Théodorou,4 Remy Burcelin1,2
1Institut National de la Santé et de la Recherche Médicale (INSERM), Toulouse, France.
2Université Toulouse III - Paul Sabatier (UPS), Unité Mixte de Recherche (UMR) 1048, Institut de Maladies Métaboliques et Cardiovasculaires (I2MC), Toulouse Cedex 4, France.
3Université de Toulouse III – Paul Sabatier, UPS, LU49, Adhésion Bactérienne et Formation de Biofilms, Toulouse Cedex 9, France.
4Neuro-Gastroenterology and Nutrition Unit, UMR INRA/EI-Purpan, Toulouse Cedex 3, France.
5Plateforme Bio-informatique Toulouse Genopole, UBIA INRA, Castanet-Tolosan Cedex, France.
6GENOTOUL Platform, INRA Chemin de Borde-Rouge, Auzeville, France.
7Université de Toulouse III – Paul Sabatier, INSA, UPS, INP, LISBP, Toulouse, France.
8CNRS, UMR5504, Toulouse, France.
9INRA, UMR792 Ingénierie des Systèmes Biologiques et des Procédés, Toulouse, France. 10Institut Universitaire de France, Paris, France. 11Rangueil Hospital, Department of Therapeutics, Toulouse, France.
Gut, hardcopy version, April 2012, http://dx.doi.org/10.1136/gutjnl-2011-301012.
Research contact
Matteo Serino
05 61 32 56 12
matteo.serino@inserm.fr
Press Contact
Laure Mégas
presse@inserm.fr
Journal
Gut