Scientists have known for the past twenty
years that a fibre-rich diet protects the organism against obesity and diabetes
but the mechanisms involved have so far eluded them.
A French-Swedish team including researchers
from CNRS, Inserm and the Université Claude Bernard Lyon 1 has succeeded in
elucidating this mechanism, which involves the intestinal flora and the ability
of the intestine to produce glucose between meals.
These results, published in the journal
Cell, also clarify the role of the intestine and its associated microorganisms
in maintaining glycaemia. They will give rise to new dietary recommendations to
prevent diabetes and obesity.
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The enzyme responsible for the final
reaction in intestinal glucose production is highlighted by immuno-fluorescence
(red) using confocal microscopy.
Most sweet fruit and many vegetables such
as cabbage or beans are rich in so-called fermentable fibres. Such fibres
cannot be digested directly by the intestine but are instead fermented by
intestinal bacteria into short-chain fatty acids such as propionate and
butyrate, which can in fact be assimilated by our bodies.
The protective effect of these fibres is
well known to researchers: animals fed a fibre-rich diet become less fat and
are less likely to develop diabetes than animals fed a fibre-free diet.
Nevertheless, the mechanism behind this effect has until now remained a
The team headed by Gilles Mithieux, CNRS
researcher in the “Nutrition et Cerveau” unit , wondered whether this mechanism
could be linked to the capacity of the intestine to produce glucose. The
intestine is in fact capable of synthesizing this sugar and releasing it into
the blood stream between meals and at night.
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However, glucose has particular properties:
it is detected by the nerves in the walls of the portal vein (which collects
the blood coming from the intestine), which in turn sends a nerve signal to the
brain. In response, the brain triggers a range of protective effects against
diabetes and obesity: the sensation of hunger fades, energy expenditure at rest
is enhanced and, last but not least, the liver produces less glucose.
In order to make the connection between
fermentable fibres and the production of glucose by the intestine, the
researchers subjected rats and mice to diets enriched with fermentable fibres,
or with propionate or butyrate.
They then observed a strong induction of
the expression of genes and enzymes responsible for the synthesis of glucose in
the intestine. They showed that the intestine of these animals used propionate
as precursor to increase the production of glucose.
Mice fed a fat- and sugar-rich diet, but
supplemented with fibres, became less fat than control mice and were also
protected against the development of diabetes thanks to significantly increased
sensitivity to insulin.
The researchers repeated the experiment
with mice whose intestine’s ability to produce glucose had been suppressed by
No protective effect
No protective effect was then observed:
these mice became fat and developed diabetes like those fed a fibre-free diet.
It is therefore the production of glucose by the intestine from propionate and
butyrate that is behind the positive effects of fermentable fibres on the
Apart from this previously unknown
mechanism, this work sheds light on the role of the intestinal flora which, by
fermenting dietary fibre, provides the intestine with precursors to produce
glucose. It also demonstrates the importance of the intestine in the regulation
of glucose in the body. Finally, these findings should make it possible to
propose nutritional guidelines and to highlight new therapeutic targets for
preventing or treating diabetes and obesity.
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