How do we control satiation?
It is provided by a complex work of receptors in the gastrointestinal canal that feels it’s wall dilatation by the food masses and sends a signal to the brain to induce satiation and satiety. Intestinal endocrine L-cells are among the major parts of the gut-brain axis. These cells produce anorectic peptide hormones glucagon-like peptide-1 (GLP-1) and peptide YY (PYY) as a response to the food intake. This process is described in our short MoA medical animation video. GLP-1, when released into the bloodstream, affects pancreatic β-cells, which secrete insulin, a hormone that controls the glucose level; decreases gastric emptying; increases satiation. Furthermore, GI motility is reduced and food consumption decreased by PYY. L-cells also seems to have precise nutrient-perception receptors that is responsible for the direct detection of macronutrients. This mechanism takes place in pathways that control decreasing the appetite and raise energy outlay. The nutrient-perception mechanisms could be used as a basic principle for the discovery of medicines to manage obesity and metabolic disease.
About L-cells and GLP-1
The L-cells are concentrated mostly in the mucosal layer of the bowel, and, as said before, are the main source of GLP-1. This enteral hormone is enciphered by a glucagon gene. Proglucagon is a precursor peptide that goes through tissue-determined posttranslational processing before becoming GLP-1. Interesting fact, proglucagon transforms into glucagon, in the pancreatic α-cells. Moreover, not only GLP-1 is generated from proglucagon in the intestine, but also GLP-2, a hormone that regulates epithelial cell proliferation and regeneration, oxyntomodulin, and glicentin. At physiological concentrations, GLP-2 and glucagon have no interactions with the GLP-1, despite some structural similarities to GLP-1. Two enteral hormones (GLP-1 and glucose-dependent insulinotropic peptide) emitted by L-cells and the K-cells are called incretins because their secretion depends on the time you have a meal, enrolling glucose-dependent insulin secretion.