| Literature DB >> 23230114 |
Abstract
The field of intestinal physiology has been transformed by the discovery that nutrient-sensitive chemosensors are strategically positioned within the gastrointestinal tract to regulate nutrient absorption and gut hormone secretion. It is well established that the composition of the diet modulates the absorptive capacity of the intestine and the secretion of gut peptides including glucoinsulinotropic polypeptide, glucagon-like peptide-1, and peptide YY. Through these mechanisms chemosensors, including nutrient transporters and G protein coupled receptors, are able to regulate cellular energy uptake, expenditure, and homeostasis in intestine. Over the past few decades, the molecular identities for some of the chemosensors that respond to the arrival of dietary nutrients have been revealed. This review summarizes the current understanding of intestinal chemosensors in nutrition and their ability to regulate cellular energy homeostasis through the expression of nutrient transporters and the secretion of gut peptides. In both humans and animals, this raises exciting possibilities to beneficially manipulate whole body metabolic processes. In humans, malnutrition or metabolic diseases, such as obesity and type 2 diabetes, may result from impaired intestinal chemosensing. Therefore, intestinal chemosensors associated with the neuroendocrine control of metabolism are considered targets for nutritional and pharmacological intervention, with the potential to manipulate the nutritional status of actively growing or elderly individuals and/or restore energy homeostasis during metabolic disease. In the animal world, targeting intestinal chemosensors to increase energy supply in animals is likely to affect feed consumption, gut development, health, and growth efficiency. For instance, stimulating nutrient absorption at an early age may reduce incidence of intestinal disorders postweaning and this could improve feed efficiency, impacting the economic and environmental sustainability of animal-protein production.Entities:
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Year: 2012 PMID: 23230114 DOI: 10.2527/jas.2012-5906
Source DB: PubMed Journal: J Anim Sci ISSN: 0021-8812 Impact factor: 3.159