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glucagon-like peptide 1 (GLP1)

Function: - derived by cleavage from proglucagon - GLP-1 is further N-terminally truncated by post-translational processing in intestinal L cells resulting in GLP-1(7-37) - GLP-1-(7-36)amide the C-terminal amidation is neither important for the metabolism of GLP-1 nor for its effects on the endocrine pancreas - inhibits glucagon secretion - regulates gastric motility - may promote satiety - stimulates prolideration of pancreatic islet beta cells & prevents their apoptosis in culture - stimulates glucose-dependent insulin release - may stimulate glucose clearance in peripheral tissues, independent of the actions of insulin - may have growth-promoting activities on intestinal epithelium - may regulate the hypothalamic pituitary axis (HPA) via effects on LH, TSH, CRH, oxytocin, & vasopressin secretion Pharmacokinetics: - 1/2life is 1-2 minutes Expression: - plasma levels of GLP-1 rise coincident with the postprandial increase in plasma glucose - reciprocal relationship between plasma levels of GLP-1 & glucagon - GLP-1, GLP-2, oxyntomodulin & glicentin are secreted from enteroendocrine cells throughout the GI tract - GLP-1 & GLP-2 are also secreted in selected neurons in the brain - GLP-1 & GLP-2 are induced in response to nutrient ingestion Genetics: - glucagon & glucagon-like peptide-1 are produced by tissue-specific alternative post-translational processing of proglucagon Pharmacology: - exenatide (Byetta) for treatment of diabetes mellitus type 2 stimulates GLP-1 receptors - dipeptidyl dipeptidase inhibitors inhibit catabolism of GLP1 Pathology: - function may be aberrant in diabetes mellitus type 2 [2]

Related

exenatide (Byetta, AC2993, extendin-4, Gilly, Lizzie, Bydureon) glucagon-like peptide 1 receptor; GLP-1 receptor; GLP-1-R; GLP-1R (GLP1R)

General

endocrine agent incretin pancreatic hormone secretin family peptide

Properties

COMPARTMENT: plasma SECRETED-BY: endocrine cell WITHIN: intestine

Database Correlations

OMIM 138030 UniProt P01275

References

  1. prosite :accession PS00260
  2. Internal Medicine World Report 20(8):1, 2005