Institut für Ernährungswissenschaften

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    Effect of a diet rich in galactose or fructose, with or without fructooligosaccharides, on gut microbiota composition in rats
    (2022) Mhd Omar, Nor Adila; Dicksved, Johan; Kruger, Johanita; Zamaratskaia, Galia; Michaëlsson, Karl; Wolk, Alicja; Frank, Jan; Landberg, Rikard
    Recent studies suggest that a diet rich in sugars significantly affects the gut microbiota. Adverse metabolic effects of sugars may partly be mediated by alterations of gut microbiota and gut health parameters, but experimental evidence is lacking. Therefore, we investigated the effects of high intake of fructose or galactose, with/without fructooligosaccharides (FOS), on gut microbiota composition in rats and explored the association between gut microbiota and low-grade systemic inflammation. Sprague–Dawley rats (n = 6/group) were fed the following isocaloric diets for 12 weeks (% of the dry weight of the sugars or FOS): (1) starch (control), (2) fructose (50%), (3) galactose (50%), (4) starch+FOS (15%) (FOS control), (5) fructose (50%)+FOS (15%), (6) galactose (50%)+FOS (15%), and (7) starch+olive (negative control). Microbiota composition in the large intestinal content was determined by sequencing amplicons from the 16S rRNA gene; 341F and 805R primers were used to generate amplicons from the V3 and V4 regions. Actinobacteria, Verrucomicrobia, Tenericutes, and Cyanobacteria composition differed between diets. Bifidobacterium was significantly higher in all diet groups where FOS was included. Modest associations between gut microbiota and metabolic factors as well as with gut permeability markers were observed, but no associations between gut microbiota and inflammation markers were observed. We found no coherent effect of galactose or fructose on gut microbiota composition. Added FOS increased Bifidobacterium but did not mitigate potential adverse metabolic effects induced by the sugars. However, gut microbiota composition was associated with several metabolic factors and gut permeability markers which warrant further investigations.
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    Intestinal dysbiosis associated with non-nutritive sweeteners intake: an effect without a cause?
    (2025) Marongiu, Luigi; Brzozowska, Ewa; Hetjens, Svetlana; Hoelzle, Ludwig E.; Venturelli, Sascha; Brzozowska, Ewa; Laboratory of Medical Microbiology, Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Wroclaw, Poland; Hetjens, Svetlana; Department of Medical Statistics, Biomathematics and Information Processing, University Clinic Mannheim, Mannheim, Germany; Hoelzle, Ludwig E.; Department of Food Microbiology and Hygiene, Institute of Food Science and Biotechnology, University of Hohenheim, Stuttgart, Germany; Venturelli, Sascha; Department of Nutritional Biochemistry, University of Hohenheim, Stuttgart, Germany
    Non-nutritive sweeteners (NNS) are present in various commercial articles, from foodstuffs to oral hygiene products. Despite their alleged safety, mounting evidence indicates that NNS intake is associated with an alteration of intestinal bacterial populations (dysbiosis) in animals and humans. Since NNS are commercialized based on the assumption that they are not metabolized by human cells and negligible effect on bacterial, the insurgence of dysbiosis associated with NNS intake remains unexplained. The current review aims to assess the effect of selected NNS (acesulfame potassium, advantame, aspartame, neotame, saccharin, stevia, and sucralose) on the human intestinal microbiota. Findings from this review suggests that NNS intake is linked not only to alterations in human physiology but also to modifications of bacterial biochemistry, including the hindrance of quorum sensing pathways, in a species-specific manner. Moreover, there were suggestions that NNS could also affect the biology of phages, namely by binding to the active sites of proteins involved in the infection process and altering the induction rate of prophages. The studies gathered in the present review provide a framework for understanding how NNS might be connected to dysbiosis, both directly through alterations in bacterial biochemistry and indirectly through impaired phage activity.