Journal
OBESITY REVIEWS
Volume 19, Issue 4, Pages 435-451Publisher
WILEY
DOI: 10.1111/obr.12661
Keywords
hypothalamus; inflammation; microbiota; obesity
Categories
Funding
- European Union [613979, 607310]
- Spanish Ministry of Economy and Competitiveness (MINECO) [AGL2014-52101-P]
- Swedish Research Council for Medicine (Vetenskapsradet) [2016-20195]
- Dutch STW
- European College for Neuropsychopharmacology (the Nutrition Network)
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Western diets, with high consumption of simple sugars and saturated fats, contribute to the rise in the prevalence of obesity. It now seems clear that high-fat diets cause obesity, at least in part, by modifying the composition and function of the microorganisms that colonize in the gastrointestinal tract, the microbiota. The exact pathways by which intestinal microbiota contribute to obesity remain largely unknown. High-fat diet-induced alterations in intestinal microbiota have been suggested to increase energy extraction, intestinal permeability and systemic inflammation while decreasing the capability to generate obesity-suppressing short-chain fatty acids. Moreover, by increasing systemic inflammation, microglial activation and affecting vagal nerve activity, obese microbiota' indirectly influence hypothalamic gene expression and promote overeating. Because the potential of intestinal microbiota to induce obesity has been recognized, multiple ways to modify its composition and function are being investigated to provide novel preventive and therapeutic strategies against diet-induced obesity.
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