Glucagon-like peptide 1 (GLP-1): a potent gut hormone with a possible therapeutic perspective
| ISSN: |
1432-5233
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| Keywords: |
Key words Incretin ; Gastric inhibitory polypeptide ; Glucagon-like peptide 1 ; Gut hormones ; Type 2 diabetes ; Type 1 diabetes ; Obesity ; New treatment modalities
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| Source: |
Springer Online Journal Archives 1860-2000
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| Topics: |
Medicine
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| Notes: |
Abstract Glucagon-like peptide 1 (GLP-1) is a physiological incretin hormone from the lower gastrointestinal tract, partially explaining the augmented insulin response after oral compared to intravenous glucose administration in normal humans. In addition, GLP-1 also lowers glucagon concentrations, slows gastric emptying, stimulates (pro)insulin biosynthesis, and reduces food intake upon intracerebroventricular administration in animals. Therefore, GLP-1 offers some interesting perspective for the treatment of type 2, and perhaps also for type 1 diabetic patients. The other incretin hormone, gastric inhibitory polypeptide (GIP), has lost almost all its activity in type-2 diabetic patients. In contrast, GLP-1 glucose-dependently stimulates insulin secretion in type-2 diabetic patients and exogenous administration of GLP-1 ([7–37] or [7–36 amide]) in doses elevating plasma concentrations to approximately three to four times physiological postprandial levels fully normalizes fasting hyperglycaemia and reduces postprandial glycaemic increments. Due to rapid proteolytic cleavage, which results in an inactive or even antagonistic fragment, GLP-1 [9–36 amide], and to rapid elimination, the half-life of GLP-1 is too short to maintain therapeutic plasma levels for sufficient periods by subcutaneous injections of the natural peptide hormone. Current research aims to characterize GLP-1 analogues with more suitable pharmacokinetic properties than the original peptide. Given the large amount of GLP-1 present in L cells, it also appears worthwhile to search for more agents that could `mobilize' this endogenous pool of GLP-1.
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| Type of Medium: |
Electronic Resource
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| URL: |
| _version_ | 1798296009165504513 |
|---|---|
| autor | Nauck, M. A. |
| autorsonst | Nauck, M. A. |
| book_url | http://dx.doi.org/10.1007/s005920050116 |
| datenlieferant | nat_lic_papers |
| hauptsatz | hsatz_simple |
| identnr | NLM206143532 |
| iqvoc_descriptor_keyword | iqvoc_00000098:Gut |
| iqvoc_descriptor_title | iqvoc_00000098:gut |
| issn | 1432-5233 |
| journal_name | Acta diabetologica |
| materialart | 1 |
| notes | Abstract Glucagon-like peptide 1 (GLP-1) is a physiological incretin hormone from the lower gastrointestinal tract, partially explaining the augmented insulin response after oral compared to intravenous glucose administration in normal humans. In addition, GLP-1 also lowers glucagon concentrations, slows gastric emptying, stimulates (pro)insulin biosynthesis, and reduces food intake upon intracerebroventricular administration in animals. Therefore, GLP-1 offers some interesting perspective for the treatment of type 2, and perhaps also for type 1 diabetic patients. The other incretin hormone, gastric inhibitory polypeptide (GIP), has lost almost all its activity in type-2 diabetic patients. In contrast, GLP-1 glucose-dependently stimulates insulin secretion in type-2 diabetic patients and exogenous administration of GLP-1 ([7–37] or [7–36 amide]) in doses elevating plasma concentrations to approximately three to four times physiological postprandial levels fully normalizes fasting hyperglycaemia and reduces postprandial glycaemic increments. Due to rapid proteolytic cleavage, which results in an inactive or even antagonistic fragment, GLP-1 [9–36 amide], and to rapid elimination, the half-life of GLP-1 is too short to maintain therapeutic plasma levels for sufficient periods by subcutaneous injections of the natural peptide hormone. Current research aims to characterize GLP-1 analogues with more suitable pharmacokinetic properties than the original peptide. Given the large amount of GLP-1 present in L cells, it also appears worthwhile to search for more agents that could `mobilize' this endogenous pool of GLP-1. |
| package_name | Springer |
| publikationsjahr_anzeige | 1998 |
| publikationsjahr_facette | 1998 |
| publikationsjahr_intervall | 8004:1995-1999 |
| publikationsjahr_sort | 1998 |
| publisher | Springer |
| reference | 35 (1998), S. 117-129 |
| schlagwort | Key words Incretin Gastric inhibitory polypeptide Glucagon-like peptide 1 Gut hormones Type 2 diabetes Type 1 diabetes Obesity New treatment modalities |
| search_space | articles |
| shingle_author_1 | Nauck, M. A. |
| shingle_author_2 | Nauck, M. A. |
| shingle_author_3 | Nauck, M. A. |
| shingle_author_4 | Nauck, M. A. |
| shingle_catch_all_1 | Nauck, M. A. Glucagon-like peptide 1 (GLP-1): a potent gut hormone with a possible therapeutic perspective Key words Incretin Gastric inhibitory polypeptide Glucagon-like peptide 1 Gut hormones Type 2 diabetes Type 1 diabetes Obesity New treatment modalities Key words Incretin Gastric inhibitory polypeptide Glucagon-like peptide 1 Gut hormones Type 2 diabetes Type 1 diabetes Obesity New treatment modalities Abstract Glucagon-like peptide 1 (GLP-1) is a physiological incretin hormone from the lower gastrointestinal tract, partially explaining the augmented insulin response after oral compared to intravenous glucose administration in normal humans. In addition, GLP-1 also lowers glucagon concentrations, slows gastric emptying, stimulates (pro)insulin biosynthesis, and reduces food intake upon intracerebroventricular administration in animals. Therefore, GLP-1 offers some interesting perspective for the treatment of type 2, and perhaps also for type 1 diabetic patients. The other incretin hormone, gastric inhibitory polypeptide (GIP), has lost almost all its activity in type-2 diabetic patients. In contrast, GLP-1 glucose-dependently stimulates insulin secretion in type-2 diabetic patients and exogenous administration of GLP-1 ([7–37] or [7–36 amide]) in doses elevating plasma concentrations to approximately three to four times physiological postprandial levels fully normalizes fasting hyperglycaemia and reduces postprandial glycaemic increments. Due to rapid proteolytic cleavage, which results in an inactive or even antagonistic fragment, GLP-1 [9–36 amide], and to rapid elimination, the half-life of GLP-1 is too short to maintain therapeutic plasma levels for sufficient periods by subcutaneous injections of the natural peptide hormone. Current research aims to characterize GLP-1 analogues with more suitable pharmacokinetic properties than the original peptide. Given the large amount of GLP-1 present in L cells, it also appears worthwhile to search for more agents that could `mobilize' this endogenous pool of GLP-1. 1432-5233 14325233 Springer |
| shingle_catch_all_2 | Nauck, M. A. Glucagon-like peptide 1 (GLP-1): a potent gut hormone with a possible therapeutic perspective Key words Incretin Gastric inhibitory polypeptide Glucagon-like peptide 1 Gut hormones Type 2 diabetes Type 1 diabetes Obesity New treatment modalities Key words Incretin Gastric inhibitory polypeptide Glucagon-like peptide 1 Gut hormones Type 2 diabetes Type 1 diabetes Obesity New treatment modalities Abstract Glucagon-like peptide 1 (GLP-1) is a physiological incretin hormone from the lower gastrointestinal tract, partially explaining the augmented insulin response after oral compared to intravenous glucose administration in normal humans. In addition, GLP-1 also lowers glucagon concentrations, slows gastric emptying, stimulates (pro)insulin biosynthesis, and reduces food intake upon intracerebroventricular administration in animals. Therefore, GLP-1 offers some interesting perspective for the treatment of type 2, and perhaps also for type 1 diabetic patients. The other incretin hormone, gastric inhibitory polypeptide (GIP), has lost almost all its activity in type-2 diabetic patients. In contrast, GLP-1 glucose-dependently stimulates insulin secretion in type-2 diabetic patients and exogenous administration of GLP-1 ([7–37] or [7–36 amide]) in doses elevating plasma concentrations to approximately three to four times physiological postprandial levels fully normalizes fasting hyperglycaemia and reduces postprandial glycaemic increments. Due to rapid proteolytic cleavage, which results in an inactive or even antagonistic fragment, GLP-1 [9–36 amide], and to rapid elimination, the half-life of GLP-1 is too short to maintain therapeutic plasma levels for sufficient periods by subcutaneous injections of the natural peptide hormone. Current research aims to characterize GLP-1 analogues with more suitable pharmacokinetic properties than the original peptide. Given the large amount of GLP-1 present in L cells, it also appears worthwhile to search for more agents that could `mobilize' this endogenous pool of GLP-1. 1432-5233 14325233 Springer |
| shingle_catch_all_3 | Nauck, M. A. Glucagon-like peptide 1 (GLP-1): a potent gut hormone with a possible therapeutic perspective Key words Incretin Gastric inhibitory polypeptide Glucagon-like peptide 1 Gut hormones Type 2 diabetes Type 1 diabetes Obesity New treatment modalities Key words Incretin Gastric inhibitory polypeptide Glucagon-like peptide 1 Gut hormones Type 2 diabetes Type 1 diabetes Obesity New treatment modalities Abstract Glucagon-like peptide 1 (GLP-1) is a physiological incretin hormone from the lower gastrointestinal tract, partially explaining the augmented insulin response after oral compared to intravenous glucose administration in normal humans. In addition, GLP-1 also lowers glucagon concentrations, slows gastric emptying, stimulates (pro)insulin biosynthesis, and reduces food intake upon intracerebroventricular administration in animals. Therefore, GLP-1 offers some interesting perspective for the treatment of type 2, and perhaps also for type 1 diabetic patients. The other incretin hormone, gastric inhibitory polypeptide (GIP), has lost almost all its activity in type-2 diabetic patients. In contrast, GLP-1 glucose-dependently stimulates insulin secretion in type-2 diabetic patients and exogenous administration of GLP-1 ([7–37] or [7–36 amide]) in doses elevating plasma concentrations to approximately three to four times physiological postprandial levels fully normalizes fasting hyperglycaemia and reduces postprandial glycaemic increments. Due to rapid proteolytic cleavage, which results in an inactive or even antagonistic fragment, GLP-1 [9–36 amide], and to rapid elimination, the half-life of GLP-1 is too short to maintain therapeutic plasma levels for sufficient periods by subcutaneous injections of the natural peptide hormone. Current research aims to characterize GLP-1 analogues with more suitable pharmacokinetic properties than the original peptide. Given the large amount of GLP-1 present in L cells, it also appears worthwhile to search for more agents that could `mobilize' this endogenous pool of GLP-1. 1432-5233 14325233 Springer |
| shingle_catch_all_4 | Nauck, M. A. Glucagon-like peptide 1 (GLP-1): a potent gut hormone with a possible therapeutic perspective Key words Incretin Gastric inhibitory polypeptide Glucagon-like peptide 1 Gut hormones Type 2 diabetes Type 1 diabetes Obesity New treatment modalities Key words Incretin Gastric inhibitory polypeptide Glucagon-like peptide 1 Gut hormones Type 2 diabetes Type 1 diabetes Obesity New treatment modalities Abstract Glucagon-like peptide 1 (GLP-1) is a physiological incretin hormone from the lower gastrointestinal tract, partially explaining the augmented insulin response after oral compared to intravenous glucose administration in normal humans. In addition, GLP-1 also lowers glucagon concentrations, slows gastric emptying, stimulates (pro)insulin biosynthesis, and reduces food intake upon intracerebroventricular administration in animals. Therefore, GLP-1 offers some interesting perspective for the treatment of type 2, and perhaps also for type 1 diabetic patients. The other incretin hormone, gastric inhibitory polypeptide (GIP), has lost almost all its activity in type-2 diabetic patients. In contrast, GLP-1 glucose-dependently stimulates insulin secretion in type-2 diabetic patients and exogenous administration of GLP-1 ([7–37] or [7–36 amide]) in doses elevating plasma concentrations to approximately three to four times physiological postprandial levels fully normalizes fasting hyperglycaemia and reduces postprandial glycaemic increments. Due to rapid proteolytic cleavage, which results in an inactive or even antagonistic fragment, GLP-1 [9–36 amide], and to rapid elimination, the half-life of GLP-1 is too short to maintain therapeutic plasma levels for sufficient periods by subcutaneous injections of the natural peptide hormone. Current research aims to characterize GLP-1 analogues with more suitable pharmacokinetic properties than the original peptide. Given the large amount of GLP-1 present in L cells, it also appears worthwhile to search for more agents that could `mobilize' this endogenous pool of GLP-1. 1432-5233 14325233 Springer |
| shingle_title_1 | Glucagon-like peptide 1 (GLP-1): a potent gut hormone with a possible therapeutic perspective |
| shingle_title_2 | Glucagon-like peptide 1 (GLP-1): a potent gut hormone with a possible therapeutic perspective |
| shingle_title_3 | Glucagon-like peptide 1 (GLP-1): a potent gut hormone with a possible therapeutic perspective |
| shingle_title_4 | Glucagon-like peptide 1 (GLP-1): a potent gut hormone with a possible therapeutic perspective |
| sigel_instance_filter | dkfz geomar wilbert ipn albert fhp |
| source_archive | Springer Online Journal Archives 1860-2000 |
| timestamp | 2024-05-06T09:45:17.031Z |
| titel | Glucagon-like peptide 1 (GLP-1): a potent gut hormone with a possible therapeutic perspective |
| titel_suche | Glucagon-like peptide 1 (GLP-1): a potent gut hormone with a possible therapeutic perspective |
| topic | WW-YZ |
| uid | nat_lic_papers_NLM206143532 |