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NutrInsight • Satiety: News Insights
Role of gut fermentation
A role for bacterial metabolites released upon prebiotic/dietary fibre fermentation has been suggested in the control of the gut endocrine function. The fermentation of CHO in the gut produces short-chain free fatty acids (SCFA): acetate, propionate, and butyrate. The bacterial fermentation of indigestible prebiotics to SCFA could in turn modulate the release of gut hormones controlling insulin release and appetite. It has been established that SCFA trigger the secretion of GLP-1 from mixed colonic cultures in vitro [Tolhurst et al., 2010].
Cell differentiation induced by prebiotics
The modulation of gut endocrine function by prebiotics in obese rats or mice involves an increase in the number of endocrine L-cells in the intestine, an effect which is correlated to bacterial changes in the gut. Endocrine L-cells must differentiate in order to express proglucagon gene, and to release various gastro-intestinal hormones and peptides among which GLP-1 and GLP-2 are relevant to energy homeostasis. While GLP-1 is a satietogenic peptide with incretin functions associated with decreases in hepatic lipids, GLP-2 is involved in intestinal cell proliferation and improved barrier function [Estall & Drucker, 2006; Hadjiyanni et al., 2009]. GLP-2 is released following food intake and plays a significant role in the adaptive regulation of bowel mass and mucosal integrity. Prebiotic-induced changes in gut microbiota are associated with increased plasma GLP-1 and enteroendocrine L-cell number in obese mice [Everard et al., 2011].
It is presently unknown by which mechanism the gut microbial environment influences L-cells differentiation. However, the production of SCFA (namely acetate, propionate) upon CHO fermentation could be involved in the increase in gut peptide secretion by endocrine cells, by interacting with specific G-coupled receptors (GPR41 and GPR43). In addition, the gut microbiota influences the production in host tissues (intestine, adipose tissue) of endocannabinoids, which are able to modulate appetite by interacting with cannabinoid receptors (CB1R) expressed in neuronal cells. Changing the gut microbiota by nutrients also influences gut motility or glycemia, which can in turn contribute to the regulation of appetite.
The gut endocannabinoid system
The endocannabinoid (eCB) system is a novel target for the control of food intake via gut microbiota manipulations. The eCB system includes at least two G-protein-coupled receptors, the endogenous agonists of these receptors, and proteins and enzymes involved in the regulation of eCB levels and action at receptors [Di Marzo, 2009]. The eCB system is quite widespread in and appears to play a pro-homeostatic role. For example, the eCB system is activated in the gut of obese mice, an effect linked to increased food intake. Gut microbiota modulate the intestinal eCB system tone, which in turn regulates gut permeability and plasma lipopolysaccharide (LPS) levels [Muccioli et al., 2010]. The gut microbiota might determine adipose tissue physiology through LPS-eCB system regulatory loops and may exert critical functions in adipose tissue plasticity in obesity. The activation of the eCB system is decreased by administration of ITF prebiotics.
Human studies
Examples of prebiotic effect on appetite and food intake
In addition to the abundant animal model literature, controlled studies of satiety effects of prebiotics in humans have been published. In a cross-over study [Cani et al., 2006a], men and women received either OFS or placebo (maltodextrin) supplements twice daily (16 g/day in total). OFS significantly increased satiety sensations at breakfast and dinner. Energy intake at breakfast and lunch were significantly decreased during the OFS treatment and total daily energy intake was 5% lower during OFS administration than placebo.
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