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 |
|