Session: FP13-GI Peptides, Beta Cells & Glycemia
Room 304 (Moscone Center)
Poster Board SAT-834
Subjects and Methods: Eight men, age (mean ± SD) 21.9 ± 2.2 yr; BMI 24 ± 1.7kg/m2were studied in a single-blind, placebo-controlled study during two overnight admissions on the Clinical Research Unit. During a euglycemic hyperinsulinemic clamp, volunteers received on one admission a graded 5-h insulin infusion (mU/kg/min): 2 (0900-0910h); 1 (0910-1100h); 0.3 (1100-1230h); 0.1 (1230-1400h); and saline infusion (1400-1530h). On a separate admission volunteers received a 6.5-hr saline infusion. Plasma acyl- and desacyl-ghrelin (using an in-house two-site sandwich assay), GH, insulin and cortisol were measured every 10 min from 0700-1530h. Data were analyzed by way of linear mixed models with Bonferroni correction to compare the last hour of each infusion period.
Results:Under euglycemic conditions, there was a significant (p<0.01) difference in the mean within-subject change in acyl-ghrelin and desacyl-ghrelin (pg/ml) concentrations between interventions during the highest insulin infusion rate (1 mU/kg/min) (mean ± SE; admission: saline; insulin: acyl-ghrelin: 34.78 ± 1.86; 19.24 ± 1.07; desacyl-ghrelin: 38.33 ± 1.36; 23.45 ± 0.94). Desacyl- (but not acyl-) ghrelin levels continued to be suppressed (p<0.01) during the next insulin infusion rate of 0.3 mU/kg/min (mean ± SE; admission: saline; insulin: 35.10 ± 1.32; 23.58 ± 0.97). The geometric mean within-subject ratio fold-change in GH levels (ng/ml) was significantly higher (p<0.05) when compared to the saline admission day during the 0.1 mU/kg/min infusion rate (mean ± SE; insulin; saline: 10.97 ± 1.12; 2.6 ± 0.5). Cortisol levels did not differ.
Conclusion: Insulin inhibits the release of acyl-and desacyl-ghrelin in healthy young men in a dose-dependent manner. The suppression of acyl-and desacyl-ghrelin has a rapid onset, but upon gradual withdrawal of insulin, the recovery of acyl-ghrelin is faster than that of desacyl-ghrelin. In addition, the recovery of ghrelin is followed by a significant increase in GH.
Disclosure: MOT: Founder, Ammonett Pharma, Recipient Award, Novo Nordisk, Advisory Group Member, Pfizer, Inc., Advisory Group Member, Ipsen, Advisory Group Member, Chaisma. Nothing to Disclose: RMN, JL, SSP, LSF, JP, BDG
*Please take note of The Endocrine Society's News Embargo Policy at http://www.endo-society.org/endo2013/media.cfm
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