| Abstract |
This thesis supports the hypothesis that gut microbiota can be viewed as an ‘exteriorised organ’ that contributes to energy metabolism and the modulation of our immune system. Following Koch’s postulates, it has now been shown that gut microbiota are associated with metabolic disease and that these microbiota can be isolated from a diseased organism (e.g. visceral adipose tissue). The third postulate and ultimate proof of causality have to come from trials showing beneficial effects of treatment with identified bacterial strains aimed at improving insulin sensitivity in humans.
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