Abstract
Sensing of nutrients by chemosensory cells in the gastrointestinal tract plays a key role in transmitting food-related signals, linking information about the composition of ingested foods to digestive processes. In recent years, a number of G protein-coupled receptors (GPCR) responsive to a range of nutrients have been identified. Many are localised to intestinal enteroendocrine (chemosensory) cells, promoting hormonal and neuronal signalling locally, centrally and to the periphery. The field of gut sensory systems is relatively new and still evolving. Despite huge interest in these nutrient-sensing GPCR, both as sensors for nutritional status and targets for preventing the development of metabolic diseases, major challenges remain to be resolved. However, the gut expressed sweet taste receptor, resident in L-enteroendocrine cells and responsive to dietary sweetener additives, has already been successfully explored and utilised as a therapeutic target, treating weaning-related disorders in young animals. In addition to sensing nutrients, many GPCR are targets for drugs used in clinical practice. As such these receptors, in particular those expressed in L-cells, are currently being assessed as potential new pathways for treating diabetes and obesity. Furthermore, growing recognition of gut chemosensing of microbial-produced SCFA acids has led further attention to the association between nutrition and development of chronic disorders focusing on the relationship between nutrients, gut microbiota and health. The central importance of gut nutrient sensing in the control of gastrointestinal physiology, health promotion and gut-brain communication offers promise that further therapeutic successes and nutritional recommendations will arise from research in this area.
Highlights
Sensing of nutrients by chemosensory cells in the gastrointestinal tract plays a key role in transmitting food-related signals, linking information about the composition of ingested foods to digestive processes
In 2005, we reported, for the first time, that the heterodimeric sweet taste receptor T1R2-T1R3, previously characterised in the lingual epithelium, is expressed in gut enteroendocrine cell (EEC), and proposed that it acts as the intestinal glucose sensor[15]
The total number of EEC, the expression of T1R2 and levels of gut hormones including glucagon-like peptide (GLP)-1, GLP-2 and glucose-dependent insulinotropic peptide (GIP) are all significantly reduced in the intestine of diabetic individuals[4,23,25]
Summary
Sensing of nutrients by chemosensory cells in the gastrointestinal tract plays a key role in transmitting food-related signals, linking information about the composition of ingested foods to digestive processes. The total number of EEC, the expression of T1R2 and levels of gut hormones including GLP-1, GLP-2 and GIP are all significantly reduced in the intestine of diabetic individuals[4,23,25] It appears that in type 2 diabetes, deregulation of intestinal glucose sensing and downstream signalling may play a role in the observed overexpression of intestinal SGLT1. Proteins are digested by pancreatic and brush border membrane proteases to di-tri-oligopeptides and amino acids There are these products that likely target EEC stimulating secretion of a range of gut hormones including CCK, GLP-1 and PYY[38]. The satiety effects associated with high-protein diets can be mediated by sensing of the amino acid constituents of proteins
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