title: Does GLP-1 suppress its own basal secretion?
abstract: OBJECTIVE
  Negative feedback controls in endocrine regulatory systems are well recognized. The incretins and their role in glucose regulation have been of major interest recently. Whether the same negative control system applies to the regulation of incretin secretion is not clear. We sought to examine the hypothesis that exogenous administration of glucagon like peptide-1, GLP-1(7-36) amide or its metabolite GLP-1(9-36) amide, reduces the endogenous basal release of this incretin.
  
  
  METHODS
  We evaluated the endogenous basal release of GLP-1 using two separate study designs. In protocol A we examined the GLP-1(7-36) amide levels during the infusion of GLP-1(9-36) amide. In protocol B, we used PYY and GLP-2 as biomarkers for the endogenous basal release of GLP-1(7-36) amide and assessed the endogenous basal release of these two hormones during the GLP-1(7-36) infusion. Twelve lean and 12 obese subjects were enrolled in protocol A and 10 obese volunteers in protocol B.
  
  
  RESULTS
  The plasma levels of GLP-1(7-36) amide in protocol A and PYY and GLP-2 in protocol B remained unchanged during the exogenous infusion of GLP-1(9-36) and GLP-1(7-36) amide, respectively.
  
  
  CONCLUSIONS
  The negative feedback control system as described by inhibition of the release of endogenous hormone while infusing it exogenously was not observed for the basal secretion of GLP-1(7-36) amide.
authors.affiliation: a ICON Early Phase Services, LLC , San Antonio , TX , USA .
authors.forename: Dariush
authors.initials: D
authors.lastname: Elahi
authors.affiliation: a ICON Early Phase Services, LLC , San Antonio , TX , USA .
authors.forename: Dennis A
authors.initials: DA
authors.lastname: Ruff
authors.affiliation: b Diabetes Section, National Institute on Aging , Baltimore , MD , USA .
authors.forename: Olga D
authors.initials: OD
authors.lastname: Carlson
authors.affiliation: c Department of Medicine , University of British Columbia School of Medicine , Vancouver , BC , Canada , and.
authors.forename: Graydon S
authors.initials: GS
authors.lastname: Meneilly
authors.affiliation: d Department of Medicine , Harvard Medical School and Massachusetts General Hospital , Boston , MA , USA.
authors.forename: Joel F
authors.initials: JF
authors.lastname: Habener
authors.affiliation: b Diabetes Section, National Institute on Aging , Baltimore , MD , USA .
authors.forename: Josephine M
authors.initials: JM
authors.lastname: Egan
mesh_terms: D000328:Adult; D001481:Basal Metabolism / Q000187:drug effects; D001786:Blood Glucose / Q000378:metabolism; D025461:Feedback, Physiological / Q000187:drug effects*; D005260:Female; D005934:Glucagon / Q000097:blood; D052216:Glucagon-Like Peptide 1 / Q000031:analogs & derivatives* / Q000378:metabolism* / Q000494:pharmacology; D006801:Humans; D007328:Insulin / Q000097:blood; D008297:Male; D009765:Obesity / Q000378:metabolism; D010446:Peptide Fragments / Q000494:pharmacology*; D010455:Peptides / Q000494:pharmacology*; D013851:Thinness / Q000378:metabolism
chemical_list: D001786:Blood Glucose; D007328:Insulin; D010446:Peptide Fragments; D010455:Peptides; C114437:glucagon-like peptide-1 (9-36)-amide; C055453:glucagon-like peptide 1 (7-36)amide; D052216:Glucagon-Like Peptide 1; D005934:Glucagon
keywords: GLP-1; glucose clamp; insulin; negative feedback