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Ghrelin suppresses glucose-stimulated insulin secretion and deteriorates glucose tolerance in healthy humans.

dc.contributor.author Tong, Jenny
dc.contributor.author Prigeon, Ronald L
dc.contributor.author Davis, Harold W
dc.contributor.author Bidlingmaier, Martin
dc.contributor.author Kahn, Steven E
dc.contributor.author Cummings, David E
dc.contributor.author Tschöp, Matthias H
dc.contributor.author D'Alessio, David
dc.coverage.spatial United States
dc.date.accessioned 2016-08-10T20:49:01Z
dc.date.issued 2010-09
dc.identifier http://www.ncbi.nlm.nih.gov/pubmed/20584998
dc.identifier db10-0504
dc.identifier.uri https://hdl.handle.net/10161/12641
dc.description.abstract OBJECTIVE: The orexigenic gut hormone ghrelin and its receptor are present in pancreatic islets. Although ghrelin reduces insulin secretion in rodents, its effect on insulin secretion in humans has not been established. The goal of this study was to test the hypothesis that circulating ghrelin suppresses glucose-stimulated insulin secretion in healthy subjects. RESEARCH DESIGN AND METHODS: Ghrelin (0.3, 0.9 and 1.5 nmol/kg/h) or saline was infused for more than 65 min in 12 healthy patients (8 male/4 female) on 4 separate occasions in a counterbalanced fashion. An intravenous glucose tolerance test was performed during steady state plasma ghrelin levels. The acute insulin response to intravenous glucose (AIRg) was calculated from plasma insulin concentrations between 2 and 10 min after the glucose bolus. Intravenous glucose tolerance was measured as the glucose disappearance constant (Kg) from 10 to 30 min. RESULTS: The three ghrelin infusions raised plasma total ghrelin concentrations to 4-, 15-, and 23-fold above the fasting level, respectively. Ghrelin infusion did not alter fasting plasma insulin or glucose, but compared with saline, the 0.3, 0.9, and 1.5 nmol/kg/h doses decreased AIRg (2,152 +/- 448 vs. 1,478 +/- 2,889, 1,419 +/- 275, and 1,120 +/- 174 pmol/l) and Kg (0.3 and 1.5 nmol/kg/h doses only) significantly (P < 0.05 for all). Ghrelin infusion raised plasma growth hormone and serum cortisol concentrations significantly (P < 0.001 for both), but had no effect on glucagon, epinephrine, or norepinephrine levels (P = 0.44, 0.74, and 0.48, respectively). CONCLUSIONS: This is a robust proof-of-concept study showing that exogenous ghrelin reduces glucose-stimulated insulin secretion and glucose disappearance in healthy humans. Our findings raise the possibility that endogenous ghrelin has a role in physiologic insulin secretion, and that ghrelin antagonists could improve beta-cell function.
dc.language eng
dc.publisher American Diabetes Association
dc.relation.ispartof Diabetes
dc.relation.isversionof 10.2337/db10-0504
dc.subject Adolescent
dc.subject Adult
dc.subject Blood Glucose
dc.subject Female
dc.subject Ghrelin
dc.subject Glucose
dc.subject Glucose Tolerance Test
dc.subject Growth Hormone
dc.subject Humans
dc.subject Hydrocortisone
dc.subject Insulin
dc.subject Male
dc.subject Middle Aged
dc.subject Reference Values
dc.subject Young Adult
dc.title Ghrelin suppresses glucose-stimulated insulin secretion and deteriorates glucose tolerance in healthy humans.
dc.type Journal article
duke.contributor.id Tong, Jenny|0662917
duke.contributor.id D'Alessio, David|0644530
pubs.author-url http://www.ncbi.nlm.nih.gov/pubmed/20584998
pubs.begin-page 2145
pubs.end-page 2151
pubs.issue 9
pubs.organisational-group Clinical Science Departments
pubs.organisational-group Duke
pubs.organisational-group Duke Molecular Physiology Institute
pubs.organisational-group Institutes and Centers
pubs.organisational-group Medicine
pubs.organisational-group Medicine, Endocrinology, Metabolism, and Nutrition
pubs.organisational-group School of Medicine
pubs.publication-status Published
pubs.volume 59
dc.identifier.eissn 1939-327X
duke.contributor.orcid D'Alessio, David|0000-0003-4155-4870


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