Incretin: Difference between revisions
Created page with "{{Short description|Group of gastrointestinal hormones}} thumb|350px|right|GLP-1 and DPP-4 inhibitors '''Incretins''' are a group of metabolic hormones that stimulate a decrease in blood glucose levels. Incretins are released after eating and augment the secretion of insulin released from pancreatic beta cells of the islets of Langerhans by a blood-glucose–dependent mechanism. Some inc..." |
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{{Short description|Group of gastrointestinal hormones}} | {{Short description|Group of gastrointestinal hormones}} | ||
[[Image:Incretins and DPP 4 inhibitors.svg|thumb|350px|right|GLP-1 and DPP-4 inhibitors]] | [[Image:Incretins and DPP 4 inhibitors.svg|thumb|350px|right|GLP-1 and DPP-4 inhibitors]] | ||
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'''Incretins''' are a group of [[metabolic]] [[hormone]]s that stimulate a decrease in blood glucose levels. Incretins are released after eating and augment the secretion of [[insulin]] released from pancreatic [[beta cells]] of the [[islets of Langerhans]] by a [[blood glucose|blood-glucose]]–dependent mechanism. | '''Incretins''' are a group of [[metabolic]] [[hormone]]s that stimulate a decrease in blood glucose levels. Incretins are released after eating and augment the secretion of [[insulin]] released from pancreatic [[beta cells]] of the [[islets of Langerhans]] by a [[blood glucose|blood-glucose]]–dependent mechanism. | ||
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Some incretins ([[GLP-1]]) also inhibit [[glucagon]] release from the [[alpha cell]]s of the [[islets of Langerhans]]. In addition, they slow the rate of absorption of nutrients into the blood stream by reducing gastric emptying and may directly reduce food intake. The two main candidate peptides that fulfill criteria for an incretin are the intestinal [[peptide]]s [[glucagon-like peptide-1]] (GLP-1) and [[gastric inhibitory peptide]] (GIP, also known as: glucose-dependent insulinotropic polypeptide). GIP is produced and secreted into the blood circulation by [[Enteroendocrine cell#K cell|K cells]], i.e., single cells located in the mucosa of the [[upper gastrointestinal tract]]'s [[duodenum]] and upper [[jejunum]] while GLP1 is produced and secreted into the blood by [[Enteroendocrine cell#L cell|L cells]] located in the mucosa of the [[lower gastrointestinal tract]]s [[small intestine|small]] and [[large intestine]]s. [[Short-chain fatty acids]] (primarily [[acetic acid|acetic]], [[propionic acid|propionic]], and [[butyric acid]]s), which [[Microbiota|microganisms]] form in the intestines, bind to the [[FFAR2]] and [[FFAR3]] receptors on K cells and L cells to stimulate their respective production and secretion of GIP and GLP-1. Both GLP-1 and GIP are rapidly inactivated by the enzyme [[dipeptidyl peptidase-4]] (DPP-4) and are members of the glucagon peptide superfamily. | Some incretins ([[GLP-1]]) also inhibit [[glucagon]] release from the [[alpha cell]]s of the [[islets of Langerhans]]. In addition, they slow the rate of absorption of nutrients into the blood stream by reducing gastric emptying and may directly reduce food intake. The two main candidate peptides that fulfill criteria for an incretin are the intestinal [[peptide]]s [[glucagon-like peptide-1]] (GLP-1) and [[gastric inhibitory peptide]] (GIP, also known as: glucose-dependent insulinotropic polypeptide). GIP is produced and secreted into the blood circulation by [[Enteroendocrine cell#K cell|K cells]], i.e., single cells located in the mucosa of the [[upper gastrointestinal tract]]'s [[duodenum]] and upper [[jejunum]] while GLP1 is produced and secreted into the blood by [[Enteroendocrine cell#L cell|L cells]] located in the mucosa of the [[lower gastrointestinal tract]]s [[small intestine|small]] and [[large intestine]]s. [[Short-chain fatty acids]] (primarily [[acetic acid|acetic]], [[propionic acid|propionic]], and [[butyric acid]]s), which [[Microbiota|microganisms]] form in the intestines, bind to the [[FFAR2]] and [[FFAR3]] receptors on K cells and L cells to stimulate their respective production and secretion of GIP and GLP-1. Both GLP-1 and GIP are rapidly inactivated by the enzyme [[dipeptidyl peptidase-4]] (DPP-4) and are members of the glucagon peptide superfamily. | ||
== Medical uses == | == Medical uses == <!--T:4--> | ||
[[Medication]]s based on incretins are used in the treatment of [[diabetes mellitus type 2]]. | [[Medication]]s based on incretins are used in the treatment of [[diabetes mellitus type 2]]. | ||
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Several long-lasting [[Glucagon-like peptide-1 receptor agonist|GLP-1 analogs]] having insulinotropic activity have been developed, and several, including [[dulaglutide]] (Trulicity), [[exenatide]] (Byetta), [[liraglutide]] (Victoza), [[semaglutide]] (Ozempic, Wegovy and Rybelsus) and exenatide extended-release (Bydureon), have been approved for use in the U.S. | Several long-lasting [[Glucagon-like peptide-1 receptor agonist|GLP-1 analogs]] having insulinotropic activity have been developed, and several, including [[dulaglutide]] (Trulicity), [[exenatide]] (Byetta), [[liraglutide]] (Victoza), [[semaglutide]] (Ozempic, Wegovy and Rybelsus) and exenatide extended-release (Bydureon), have been approved for use in the U.S. | ||
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Another approach is to inhibit [[dipeptidyl peptidase-4|DPP-4]], the enzyme that inactivates GLP-1 and GIP. Several [[DPP-4 inhibitors]] that can be taken orally as tablets have been developed. | Another approach is to inhibit [[dipeptidyl peptidase-4|DPP-4]], the enzyme that inactivates GLP-1 and GIP. Several [[DPP-4 inhibitors]] that can be taken orally as tablets have been developed. | ||
== Incretin effect == | == Incretin effect == <!--T:7--> | ||
The incretin effect describes the phenomenon whereby oral glucose intake elicits a higher insulin response compared to intravenously introduced glucose that produces the same levels of serum glucose levels. | The incretin effect describes the phenomenon whereby oral glucose intake elicits a higher insulin response compared to intravenously introduced glucose that produces the same levels of serum glucose levels. | ||
== History == | == History == <!--T:8--> | ||
In 1932, [[Belgians|Belgian]] [[physiologist]] Jean La Barre used the word "incretin" for a [[Gastrointestinal hormone|gut hormone]], which stimulates the [[Pancreatic islets|endocrine pancreas]] including [[insulin]] release. He also proposed that such incretins could be used as a treatment for diabetes mellitus. | In 1932, [[Belgians|Belgian]] [[physiologist]] Jean La Barre used the word "incretin" for a [[Gastrointestinal hormone|gut hormone]], which stimulates the [[Pancreatic islets|endocrine pancreas]] including [[insulin]] release. He also proposed that such incretins could be used as a treatment for diabetes mellitus. | ||
==See also== | ==See also== <!--T:9--> | ||
* [[Secretin family]] | * [[Secretin family]] | ||
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{{二次利用|date=3 March 2024}} | {{二次利用|date=3 March 2024}} | ||
[[Category:Peptide hormones]] | [[Category:Peptide hormones]] | ||
[[Category:Intestinal hormones]] | [[Category:Intestinal hormones]] | ||
[[Category:Gastric hormones]] | [[Category:Gastric hormones]] | ||
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Latest revision as of 20:48, 11 March 2024
Incretins are a group of metabolic hormones that stimulate a decrease in blood glucose levels. Incretins are released after eating and augment the secretion of insulin released from pancreatic beta cells of the islets of Langerhans by a blood-glucose–dependent mechanism.
Some incretins (GLP-1) also inhibit glucagon release from the alpha cells of the islets of Langerhans. In addition, they slow the rate of absorption of nutrients into the blood stream by reducing gastric emptying and may directly reduce food intake. The two main candidate peptides that fulfill criteria for an incretin are the intestinal peptides glucagon-like peptide-1 (GLP-1) and gastric inhibitory peptide (GIP, also known as: glucose-dependent insulinotropic polypeptide). GIP is produced and secreted into the blood circulation by K cells, i.e., single cells located in the mucosa of the upper gastrointestinal tract's duodenum and upper jejunum while GLP1 is produced and secreted into the blood by L cells located in the mucosa of the lower gastrointestinal tracts small and large intestines. Short-chain fatty acids (primarily acetic, propionic, and butyric acids), which microganisms form in the intestines, bind to the FFAR2 and FFAR3 receptors on K cells and L cells to stimulate their respective production and secretion of GIP and GLP-1. Both GLP-1 and GIP are rapidly inactivated by the enzyme dipeptidyl peptidase-4 (DPP-4) and are members of the glucagon peptide superfamily.
Medical uses
Medications based on incretins are used in the treatment of diabetes mellitus type 2.
Several long-lasting GLP-1 analogs having insulinotropic activity have been developed, and several, including dulaglutide (Trulicity), exenatide (Byetta), liraglutide (Victoza), semaglutide (Ozempic, Wegovy and Rybelsus) and exenatide extended-release (Bydureon), have been approved for use in the U.S.
Another approach is to inhibit DPP-4, the enzyme that inactivates GLP-1 and GIP. Several DPP-4 inhibitors that can be taken orally as tablets have been developed.
Incretin effect
The incretin effect describes the phenomenon whereby oral glucose intake elicits a higher insulin response compared to intravenously introduced glucose that produces the same levels of serum glucose levels.
History
In 1932, Belgian physiologist Jean La Barre used the word "incretin" for a gut hormone, which stimulates the endocrine pancreas including insulin release. He also proposed that such incretins could be used as a treatment for diabetes mellitus.
See also
 | この記事は、クリエイティブ・コモンズ・表示・継承ライセンス3.0のもとで公表されたウィキペディアの項目Incretin(3 March 2024編集記事参照)を素材として二次利用しています。 Item:Q21438  |