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The gastrointestinal (GI) tract senses the ingestion of food and responds by signaling to the brain to promote satiation and satiety. Representing an important part of the gut-brain axis, enteroendocrine L-cells secrete the anorectic peptide hormones glucagon-like peptide-1 (GLP-1) and peptide YY (PYY) in response to the ingestion of food. The release of GLP-1 has multiple effects, including the secretion of insulin from pancreatic β-cells, decreased gastric emptying, and increased satiation. PYY also slows GI motility and reduces food intake. At least part of the gut-brain response seems to be due to direct sensing of macronutrients by L-cells, by mechanisms including specific nutrient-sensing receptors. Such receptors may represent possible pathways to target to decrease appetite and increase energy expenditure. Designing drugs or functional foods to exploit the machinery of these nutrient-sensing mechanisms may offer a potential approach for agents to treat obesity and metabolic disease.
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Eleanor Spreckley (2015) studied this question.
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