title: Control of glucose homeostasis by incretin hormones.
abstract: In humans as well as in other animal species, the ingestion of food provides the fundamental source of energy for various cellular activities. The intake of food and the ability of controlling the plasma levels of substrates for energy production involve complex mechanisms that ensure a constantly adequate supply of metabolites both in the fasting and in the fed state. A number of hormonal peptides released from the gastrointestinal (GI) tract in response to the ingestion of food have been shown to play a critical role in the postprandial control of glucose homeostasis. They are known to act through three main mechanisms of action. These include; (1) stimulation of insulin secretion of pancreatic islet (beta) cells; (2) inhibition of hepatic gluconeogenesis by suppression of glucagon secretion; and (3) inhibition of GI motility. While for some of these hormones all three mechanisms of action are utilized under physiological conditions, others preferentially use one or a combination of two mechanisms for lowering postprandial hyperglycemia. Although the term glucoincretins (or incretins, or insulinotropic hormones) etymologically only describes factors capable of inducing insulin secretion, it is more frequently used to identify a larger class of peptides that, rather than manifesting a specific mechanism of action (i.e., insulin secretion), share the ability of controlling glucose excursion in the fed state (with or without a direct insulinotropic effect). The latter more inclusive meaning, incretins, is used in this article. This review summarizes recent advances on synthesis, secretion, blood plasma patterns, and metabolism of some of the major GI regulatory peptides acting in the postprandial state.
authors.affiliation: Division of Endocrinology and Metabolism, Room B-131, Department of Medicine, Cedars-Sinai Medical Center, 8700 Beverly Blvd., Los Angeles, CA 90048, USA. perfettir@csmc.edu
authors.forename: R
authors.initials: R
authors.lastname: Perfetti
authors.forename: T A
authors.initials: TA
authors.lastname: Brown
authors.forename: R
authors.initials: R
authors.lastname: Velikina
authors.forename: S
authors.initials: S
authors.lastname: Busselen
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000378:metabolism*; D004734:Energy Metabolism; D005768:Gastrointestinal Hormones / Q000502:physiology*; D005769:Gastrointestinal Motility; D005934:Glucagon / Q000378:metabolism; D052216:Glucagon-Like Peptide 1; D004763:Glucagon-Like Peptides; D005943:Gluconeogenesis; D005947:Glucose / Q000378:metabolism*; D006706:Homeostasis; D006801:Humans; D007328:Insulin / Q000378:metabolism; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000378:metabolism; D008099:Liver / Q000378:metabolism; D010446:Peptide Fragments / Q000502:physiology
chemical_list: D001786:Blood Glucose; D005768:Gastrointestinal Hormones; D007328:Insulin; D010446:Peptide Fragments; C055453:glucagon-like peptide 1 (7-36)amide; D004763:Glucagon-Like Peptides; D052216:Glucagon-Like Peptide 1; D005934:Glucagon; D005947:Glucose