Microbiota modulation by eating patterns and diet composition: impact on food intake.

Abstract

There is accumulating evidence that the gut microbiota and its composition dynamics play a crucial role in regulating the host physiological functions and behavior. Diet composition is the primary modulator of bacterial richness and abundance in the gastrointestinal (GI) tract. Macronutrient (fat, sugar, and protein) and fiber contents are especially important in determining microbiota composition and its effect on health outcomes and behavior. In addition to food composition, time of intake and eating patterns have recently been shown to significantly affect gut bacterial makeup. Diet-driven unfavorable microbiota composition, or dysbiosis, can lead to an increased production of proinflammatory by-products such as lipopolysaccharide (LPS). Increased inflammatory potential is associated with alteration in gut permeability, resulting in elevated levels of LPS in the bloodstream, or metabolic endotoxemia. We have found that a chronic increase in circulating LPS is sufficient to induce hyperphagia in rodents. Chronic LPS treatment appears to specifically impair the gut-brain axis and vagally mediated satiety signaling. The vagus nerve relays information on the quantity and quality of nutrients in the GI tract to the nucleus of solitary tract in the brain stem. There is evidence that microbiota dysbiosis is associated with remodeling of the vagal afferent pathway and that normalizing the microbiota composition in rats fed a high-fat diet is sufficient to prevent vagal remodeling. Taken together, these data support a role for the microbiota in regulating gut-brain communication and eating behavior. Bacteria-originating inflammation may play a key role in impairment of diet-driven satiety and the development of hyperphagia.