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 make up. Diet-driven unfavorable microbiota composition or dysbiosis can lead to an increased production of pro-inflammatory byproducts 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 brainstem. There is evidence that microbiota dysbiosis is associated with remodeling of the vagal afferent pathway and that normalizing the microbiota composition in high fat diet (HFD) fed rats 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.

Potato-Resistant Starch Supplementation Improves Microbiota Dysbiosis, Inflammation, and Gut–Brain Signaling in High Fat-Fed Rats

“…Potato RS supplementation prevented diet-driven dysbiosis and maintained vagal NTS innervation pattern and sensitivity to gut satiety peptide CCK. Reduced sensitivity of post-ingestive negative feedback may explain the maintenance of hyperphagia in HF but not HFRS rodents [4].…”

“…There is accumulating evidence that the chronic low-grade inflammation characteristic of obesity is at least partially controlled by the gut microbiota [3]. The gastrointestinal (GI) tract is home to over 10 14 microorganisms, primarily bacteria, and microbiota makeup can influence host physiology and behavior [4]. Microbiota composition changes with diet and is especially responsive to/can be modulated by dietary fats [5,6], sugars [7], and fibers [5,8].…”

Lignans and Gut Microbiota: An Interplay Revealing Potential Health Implications

“…Diet represents one of the main factors that can modulate the bacterial richness and abundance in the gastrointestinal tract of humans and animals [42]. In this regard, the metabolites released by gut microbiota influence the physiological activities of the host [43].…”

Metabolite-Sensing G Protein-Coupled Receptors Connect the Diet-Microbiota-Metabolites Axis to Inflammatory Bowel Disease

“…In adults, dietary patterns have been proposed to alter the composition of the intestinal microbiome [22]. The major variation of gut microbiota is related to dietary changes, indicating the dominant role of diet in shaping bacterial composition [23,24]. In IBD patients, the occurrence of dysbiosis has been observed.…”