The interaction of dietary nutrients with chemoreceptors in the small intestine leads to the secretion of gut hormones, integral to the regulation of gastric emptying, energy intake and postprandial blood glucose (1). One of these receptors, initially recognised for its capacity to sense extracellular calcium, is the calcium-sensing receptor (CaSR) (2). The CaSR has subsequently been found to also sense aromatic amino acids, including L-tryptophan (L-Trp), with distinct binding sites for calcium and L-Trp (2). A substantial body of preclinical work demonstrated that the CaSR mediates gut hormone secretion in response to L-Trp, an effect promoted by extracellular calcium (2). In humans, while direct confirmation of CaSR involvement in gut hormone release remains to be thoroughly explored, intraluminal administration of calcium has been shown to enhance L-Trp-induced increases in plasma concentrations of a number of gut hormones, including cholecystokinin, glucagon-like peptide-1 and peptide YY, associated with reductions in energy intake, in both healthy individuals (3) and those with obesity (4). Moreover, recent studies have provided evidence that calcium has the capacity to also slow gastric emptying and lower postprandial blood glucose in both health and type 2 diabetes. My presentation will review evidence that calcium, alone and in combination with L-Trp, stimulates gut hormone secretion and modulates gastric emptying, appetite and glycaemia, and considers the alignment of these effects with the proposed dual-ligand engagement of the CaSR. The effects of calcium have implications for the potential development of novel, safe, low-cost, nutrient-based management strategies for obesity and type 2 diabetes.