Recent advances highlight that nutrient receptors (such as T1R1/T1R3 heterodimer, Ca sensing receptor and GPR93 for amino acids and protein, GPR40, GPR41, GPR43 and GPR120 for fatty acids, T1R2/T1R3 heterodimer for monosaccharides) are expressed in the apical face of the gut and sense nutrients in the lumen. They transduce signals for the regulation of nutrient transporter expressions in the apical face. Interestingly, they are also localised in enteroendocrine cells (EEC) and mainly exert a direct control on the secretion in the lamina propria of gastro-intestinal peptides such as cholecystokinin, glucagon-like peptide-1 and peptide YY in response to energy nutrient transit and absorption in the gut. This informs central nuclei involved in the control of feeding such as the hypothalamus and nucleus of the solitary tract of the availability of these nutrients and thus triggers adaptive responses to maintain energy homoeostasis. These nutrient receptors then have a prominent position since they manage nutrient absorption and are principally the generator of the first signal of satiation mechanisms mainly transmitted to the brain by vagal afferents. Moreover, tastants are also able to elicit gut peptides secretion via chemosensory receptors expressed in EEC. Targeting these nutrient and tastant receptors in EEC may thus be helpful to promote satiation and so to fight overfeeding and its consequences.Nutrient sensing: Gut-brain interaction: Signalling pathway Studies conducted over the last few decades have greatly improved the understanding of the mechanisms by which the gut senses luminal nutrients and the role of the gutbrain axis in the homeostatic control of energy metabolism in response to fasting or feeding ( Fig. 1 and Table 1). On the basis of very recent advances it has been shown that intestinal luminal nutrients (such as carbohydrate, fat and protein) are sensed by specific 'taste' receptors or transporters located in the membrane of cells in the intestinal epithelium (1)(2)(3) . This sensing of nutrients by enteroendocrine cells (EEC) located in the intestinal epithelium triggers the release of gastro-intestinal (GI) regulatory peptides such as ghrelin, serotonin (5-hydroxytryptamine), cholecystokinin (CCK), peptide tyrosine-tyrosine (PYY) and/or glucagon-like peptide-1 (GLP-1) as important players involved in the gut-brain connection (4)(5)(6)(7)(8) . These GI peptides can exert their regulatory effects in a paracrine way by acting locally on specific receptors of vagal afferent nerves termination that project in the nucleus of the tractus solitary at the level of the brainstem. They can also exert their regulatory effects in an endocrine fashion after entering the systemic circulation or the lymphatic system and acting on receptors located in the arcuate nucleus at the level of the hypothalamus or in the area postrema at the level of the brainstem, two areas sensitive to blood-borne signals, respectively. Because of rapid break down by proteases, the most important concentration of GI peptides is fou...

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