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Gut microbiota and energy balance

  • The microbial community populating the human digestive tract has been linked to the development of obesity, diabetes and liver diseases. Proposed mechanisms on how the gut microbiota could contribute to obesity and metabolic diseases include: (1) improved energy extraction from diet by the conversion of dietary fibre to SCFA; (2) increased intestinal permeability for bacterial lipopolysaccharides (LPS) in response to the consumption of high-fat diets resulting in an elevated systemic LPS level and low-grade inflammation. Animal studies indicate differences in the physiologic effects of fermentable and non-fermentable dietary fibres as well as differences in long-and short-term effects of fermentable dietary fibre. The human intestinal microbiome is enriched in genes involved in the degradation of indigestible polysaccharides. The extent to which dietary fibres are fermented and in which molar ratio SCFA are formed depends on their physicochemical properties and on the individual microbiome. Acetate and propionate play an importantThe microbial community populating the human digestive tract has been linked to the development of obesity, diabetes and liver diseases. Proposed mechanisms on how the gut microbiota could contribute to obesity and metabolic diseases include: (1) improved energy extraction from diet by the conversion of dietary fibre to SCFA; (2) increased intestinal permeability for bacterial lipopolysaccharides (LPS) in response to the consumption of high-fat diets resulting in an elevated systemic LPS level and low-grade inflammation. Animal studies indicate differences in the physiologic effects of fermentable and non-fermentable dietary fibres as well as differences in long-and short-term effects of fermentable dietary fibre. The human intestinal microbiome is enriched in genes involved in the degradation of indigestible polysaccharides. The extent to which dietary fibres are fermented and in which molar ratio SCFA are formed depends on their physicochemical properties and on the individual microbiome. Acetate and propionate play an important role in lipid and glucose metabolism. Acetate serves as a substrate for de novo lipogenesis in liver, whereas propionate can be utilised for gluconeogenesis. The conversion of fermentable dietary fibre to SCFA provides additional energy to the host which could promote obesity. However, epidemiologic studies indicate that diets rich in fibre rather prevent than promote obesity development. This may be due to the fact that SCFA are also ligands of free fatty acid receptors (FFAR). Activation of FFAR leads to an increased expression and secretion of enteroendocrine hormones such as glucagon-like-peptide 1 or peptide YY which cause satiety. In conclusion, the role of SCFA in host energy balance needs to be re-evaluated.zeige mehrzeige weniger

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Metadaten
Verfasserangaben:Michael BlautORCiDGND
URN:urn:nbn:de:kobv:517-opus4-414462
DOI:https://doi.org/10.25932/publishup-41446
ISSN:1866-8372
Titel des übergeordneten Werks (Englisch):Postprints der Universität Potsdam : Mathematisch Naturwissenschaftliche Reihe
Untertitel (Englisch):Role in obesity
Schriftenreihe (Bandnummer):Zweitveröffentlichungen der Universität Potsdam : Mathematisch-Naturwissenschaftliche Reihe (602)
Publikationstyp:Postprint
Sprache:Englisch
Datum der Erstveröffentlichung:14.02.2019
Erscheinungsjahr:2015
Veröffentlichende Institution:Universität Potsdam
Datum der Freischaltung:14.02.2019
Freies Schlagwort / Tag:SCFA; dietary fibre; energy extraction; gut microbiota; mouse studies; obesity
Ausgabe:602
Seitenanzahl:8
Erste Seite:227
Letzte Seite:234
Quelle:Proceedings of the Nutrition Society 74 (2015) 3, pp. 227-234 DOI: 10.1017/S0029665114001700
Organisationseinheiten:Mathematisch-Naturwissenschaftliche Fakultät
DDC-Klassifikation:6 Technik, Medizin, angewandte Wissenschaften / 63 Landwirtschaft / 630 Landwirtschaft und verwandte Bereiche
6 Technik, Medizin, angewandte Wissenschaften / 64 Hauswirtschaft und Familie / 640 Hauswirtschaft und Familie
Peer Review:Referiert
Publikationsweg:Open Access
Fördermittelquelle:Cambridge University Press (CUP)
Lizenz (Deutsch):License LogoKeine öffentliche Lizenz: Unter Urheberrechtsschutz
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