Jacqueline L. Beaudry

Abstract The body possesses critical nutrient sensors that rapidly coordinate feeding behaviour and systemic metabolism through hormones and neural pathways. In this Review, we highlight the mechanisms by which lipid sensing triggers the release of small intestinal-derived cholecystokinin, peptide YY, glucagon-like peptide 1 and glucose-dependent insulinotropic polypeptide, as well as kidney-derived growth differentiation factor 15, to regulate satiety and glucose homeostasis through the brain.

Keywords: brown adipose tissue; energy expenditure; energy metabolism; glucagon-like peptide 1; glucose control; glucose-dependent insulinotropic polypeptide; insulin sensitivity; lipid metabolism obesity; resting energy expenditure; type 2 diabetes mellitus; white adipose tissue Introduction Glucose-dependent insulinotropic polypeptide (GIP) is secreted as a 42-amino acid peptide from the K cells of the upper small intestine in response to meal ingestion (Ugleholdt et al. 2006).

Abstract Proteins activate small intestinal calcium sensing receptor (CaSR) and/or peptide transporter 1 (PepT1) to increase hormone secretion1,2,3,4,5,6,7,8, but the effect of small intestinal protein sensing and the mechanistic potential of CaSR and/or PepT1 in feeding and glucose regulation remain inconclusive.