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Ghrelin suppresses glucose-stimulated insulin secretion and deteriorates glucose tolerance in healthy humans.
Diabetes. 2010 Sep; 59(9):2145-51.D

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.

Authors+Show Affiliations

1Department of Medicine, Division of Endocrinology, University of Cincinnati, Cincinnati, Ohio, USA. jenny.tong@uc.eduNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, U.S. Gov't, Non-P.H.S.

Language

eng

PubMed ID

20584998

Citation

Tong, Jenny, et al. "Ghrelin Suppresses Glucose-stimulated Insulin Secretion and Deteriorates Glucose Tolerance in Healthy Humans." Diabetes, vol. 59, no. 9, 2010, pp. 2145-51.
Tong J, Prigeon RL, Davis HW, et al. Ghrelin suppresses glucose-stimulated insulin secretion and deteriorates glucose tolerance in healthy humans. Diabetes. 2010;59(9):2145-51.
Tong, J., Prigeon, R. L., Davis, H. W., Bidlingmaier, M., Kahn, S. E., Cummings, D. E., Tschöp, M. H., & D'Alessio, D. (2010). Ghrelin suppresses glucose-stimulated insulin secretion and deteriorates glucose tolerance in healthy humans. Diabetes, 59(9), 2145-51. https://doi.org/10.2337/db10-0504
Tong J, et al. Ghrelin Suppresses Glucose-stimulated Insulin Secretion and Deteriorates Glucose Tolerance in Healthy Humans. Diabetes. 2010;59(9):2145-51. PubMed PMID: 20584998.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Ghrelin suppresses glucose-stimulated insulin secretion and deteriorates glucose tolerance in healthy humans. AU - Tong,Jenny, AU - Prigeon,Ronald L, AU - Davis,Harold W, AU - Bidlingmaier,Martin, AU - Kahn,Steven E, AU - Cummings,David E, AU - Tschöp,Matthias H, AU - D'Alessio,David, Y1 - 2010/06/28/ PY - 2010/6/30/entrez PY - 2010/6/30/pubmed PY - 2010/9/24/medline SP - 2145 EP - 51 JF - Diabetes JO - Diabetes VL - 59 IS - 9 N2 - 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. SN - 1939-327X UR - https://www.unboundmedicine.com/medline/citation/20584998/Ghrelin_suppresses_glucose_stimulated_insulin_secretion_and_deteriorates_glucose_tolerance_in_healthy_humans_ L2 - https://diabetes.diabetesjournals.org/lookup/pmidlookup?view=long&amp;pmid=20584998 DB - PRIME DP - Unbound Medicine ER -