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Biological Pathway Taxonomy
| Preferred Name | Insulin Secretion | |
| Synonyms |
PMID: 12469359 PathwayType: signaling PMID: 22660720 Organ: pancreas PMID: 11078440 Pathway_Author: A. Nesterova ORCID:0000-0002-9448-8101 Source: Biological Process Organ_System: endocrine system CellType: insulin-secreting cell NodeType: Pathway Description: The secretion of insulin from pancreatic beta-cells is a complex process. Pathway is built manually using published studies. Notes: Headnote: The secretion of insulin from pancreatic beta-cells is a complex process. Signaling description: At the first stage insulin is synthesized as preproinsulin in the ribosomes of the rough endoplasmic reticulum.The following translation factors initiate the process: PDX1, NEUROD1, and CREB1. Preproinsulin is then cleaved to proinsulin, which is transported to the Golgi apparatus where it is packaged into secretory granules located close to the cell membrane. Proinsulin is cleaved into equimolar amounts of insulin and C-peptide (not shown) by proprotein convertase subtilisin/kexin type 1 (PCSK1) and carboxypeptidase E (CPE) in the secretory granules. The process of insulin secretion involves fusion of the secretory granules with the cell membrane and exocytosis of insulin, C-peptide, and proinsulin. The primary stimulus for insulin secretion is the beta-cell response to changes in ambient glucose.A widely accepted sequence of events involved in glucose-induced insulin secretion is as follows: glucose is transported into beta cells through facilitated diffusion of GLUT1 or GLUT2 glucose transporters. Intracellular glucose is metabolized in glycolysis to ATP. Elevation in the ATP/ADP ratio induces closure of cell-surface ATP-sensitive K channels (KCNJ11), leading to cell membrane depolarization. Cell-surface voltage-dependent Ca2 channels (VDCC) are opened facilitating extracellular Ca2 influx into the beta cell. Outcome effects: Ca2 activates PLC and the additional Ca2 portion is released from intracellular storage. Arise in free cytosolic Ca2 triggers the exocytosis of insulin. Hormones gastric inhibitory polypeptide (GIP) and glucagon (GCG) through theirs receptors GIPR and GLP1R also promote insulin release. Compounds with elevated level are highlighted in red. PMID: 21595263 PMID: 16075046 Link: https://mammal-profservices.pathwaystudio.com/app/sd?urn=urn:agi-pathway:uuid-e6534244-8510-4b59-a550-1e92e2fbaba6 |
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urn:agi-pathway:uuid-e6534244-8510-4b59-a550-1e92e2fbaba6 |
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| database_cross_reference |
PS:PathwayType PS:Description PS:Pathway_Author PS:Link PS:CellType PS:Organ_System PS:PMID PS:NodeType PS:Notes PS:Organ PS:Source
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PMID: 12469359 PathwayType: signaling PMID: 22660720 Organ: pancreas PMID: 11078440 Pathway_Author: A. Nesterova ORCID:0000-0002-9448-8101 Source: Biological Process Organ_System: endocrine system CellType: insulin-secreting cell NodeType: Pathway Description: The secretion of insulin from pancreatic beta-cells is a complex process. Pathway is built manually using published studies. Notes: Headnote: The secretion of insulin from pancreatic beta-cells is a complex process. Signaling description: At the first stage insulin is synthesized as preproinsulin in the ribosomes of the rough endoplasmic reticulum.The following translation factors initiate the process: PDX1, NEUROD1, and CREB1. Preproinsulin is then cleaved to proinsulin, which is transported to the Golgi apparatus where it is packaged into secretory granules located close to the cell membrane. Proinsulin is cleaved into equimolar amounts of insulin and C-peptide (not shown) by proprotein convertase subtilisin/kexin type 1 (PCSK1) and carboxypeptidase E (CPE) in the secretory granules. The process of insulin secretion involves fusion of the secretory granules with the cell membrane and exocytosis of insulin, C-peptide, and proinsulin. The primary stimulus for insulin secretion is the beta-cell response to changes in ambient glucose.A widely accepted sequence of events involved in glucose-induced insulin secretion is as follows: glucose is transported into beta cells through facilitated diffusion of GLUT1 or GLUT2 glucose transporters. Intracellular glucose is metabolized in glycolysis to ATP. Elevation in the ATP/ADP ratio induces closure of cell-surface ATP-sensitive K channels (KCNJ11), leading to cell membrane depolarization. Cell-surface voltage-dependent Ca2 channels (VDCC) are opened facilitating extracellular Ca2 influx into the beta cell. Outcome effects: Ca2 activates PLC and the additional Ca2 portion is released from intracellular storage. Arise in free cytosolic Ca2 triggers the exocytosis of insulin. Hormones gastric inhibitory polypeptide (GIP) and glucagon (GCG) through theirs receptors GIPR and GLP1R also promote insulin release. Compounds with elevated level are highlighted in red. PMID: 21595263 PMID: 16075046 Link: https://mammal-profservices.pathwaystudio.com/app/sd?urn=urn:agi-pathway:uuid-e6534244-8510-4b59-a550-1e92e2fbaba6
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| id |
urn:agi-pathway:uuid-e6534244-8510-4b59-a550-1e92e2fbaba6
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| label |
Insulin Secretion
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| notation |
uuid-e6534244-8510-4b59-a550-1e92e2fbaba6
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| prefLabel |
Insulin Secretion
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| treeView |
urn:agi-folder:insulin_release_and_action_on_metabolism urn:agi-folder:peptide_and_protein_hormones urn:agi-folder:endocrine_system urn:agi-folder:pancreatic_beta-cells_in_diabetes urn:agi-folder:i
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| subClassOf |
urn:agi-folder:insulin_release_and_action_on_metabolism urn:agi-folder:peptide_and_protein_hormones urn:agi-folder:endocrine_system urn:agi-folder:pancreatic_beta-cells_in_diabetes urn:agi-folder:i
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