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Decreased GH secretion and enhanced ACTH and cortisol release after ghrelin administration in Cushing's disease: comparison with GH-releasing peptide-6 (GHRP-6) and GHRH.
Pituitary. 2006; 9(2):101-7.P

Abstract

GH responsiveness to GH secretagogues (GHS) is blunted in Cushing's disease (CD), while ACTH/cortisol responses are enhanced, by mechanisms still unclear. Ghrelin, the endogenous ligand for GHS-receptors (GHS-R), increases GH, ACTH, cortisol and glucose levels in humans. This study evaluated the GH, ACTH, cortisol and glucose-releasing effects of ghrelin in CD in comparison with GHRP-6. GHRH-induced GH release was also studied. Ten patients with CD (BMI 26.9+/-1.0 kg/m(2)) and ten controls (BMI 24.4+/-1.1 kg/m(2)) received ghrelin (1 microg/kg), GHRP-6 (1 microg/kg) and GHRH (100 microg) separately. GH, ACTH, cortisol and glucose levels were measured. In CD ghrelin-induced GH (microg/L; mean +/- SE) release (peak: 7.2+/-3.0) was higher than seen with GHRP-6 (2.7+/-1.0) and GHRH (0.7+/-0.2), but lower than in controls (ghrelin: 58.3+/-12.1; GHRP-6: 22.9+/-4.8; GHRH: 11.3+/-3.7). In controls ACTH (pg/mL) release after ghrelin (79.2+/-26.8) was higher than after GHRP-6 (23.6+/-5.7). In CD these responses (ghrelin: 192+/-43; GHRP-6: 185+/-56) were similar, and enhanced compared to controls. The same was observed with cortisol. Glucose levels failed to increase after ghrelin in CD, differently than in controls. Our data suggests that hypothalamic and pituitary pathways of GH release activated by ghrelin, GHRP-6 and GHRH are deranged in chronic hypercortisolism. The increased ACTH/cortisol responses to ghrelin and GHRP-6 in CD could be mediated by overexpression of GHS-R in ACTH-secreting adenomas. Hypercortisolism apparently impairs the ability of ghrelin to increase glucose levels.

Authors+Show Affiliations

Division of Endocrinology, Universidade Federal de São Paulo, UNIFESP/EPM, Sao Paulo, Brazil. dra.silviaregina@terra.com.brNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Controlled Clinical Trial
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16832586

Citation

Correa-Silva, Silvia Regina, et al. "Decreased GH Secretion and Enhanced ACTH and Cortisol Release After Ghrelin Administration in Cushing's Disease: Comparison With GH-releasing Peptide-6 (GHRP-6) and GHRH." Pituitary, vol. 9, no. 2, 2006, pp. 101-7.
Correa-Silva SR, Nascif SO, Lengyel AM. Decreased GH secretion and enhanced ACTH and cortisol release after ghrelin administration in Cushing's disease: comparison with GH-releasing peptide-6 (GHRP-6) and GHRH. Pituitary. 2006;9(2):101-7.
Correa-Silva, S. R., Nascif, S. O., & Lengyel, A. M. (2006). Decreased GH secretion and enhanced ACTH and cortisol release after ghrelin administration in Cushing's disease: comparison with GH-releasing peptide-6 (GHRP-6) and GHRH. Pituitary, 9(2), 101-7.
Correa-Silva SR, Nascif SO, Lengyel AM. Decreased GH Secretion and Enhanced ACTH and Cortisol Release After Ghrelin Administration in Cushing's Disease: Comparison With GH-releasing Peptide-6 (GHRP-6) and GHRH. Pituitary. 2006;9(2):101-7. PubMed PMID: 16832586.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Decreased GH secretion and enhanced ACTH and cortisol release after ghrelin administration in Cushing's disease: comparison with GH-releasing peptide-6 (GHRP-6) and GHRH. AU - Correa-Silva,Silvia Regina, AU - Nascif,Sérgio Oliva, AU - Lengyel,Ana-Maria Judith, PY - 2006/7/13/pubmed PY - 2008/9/24/medline PY - 2006/7/13/entrez SP - 101 EP - 7 JF - Pituitary JO - Pituitary VL - 9 IS - 2 N2 - GH responsiveness to GH secretagogues (GHS) is blunted in Cushing's disease (CD), while ACTH/cortisol responses are enhanced, by mechanisms still unclear. Ghrelin, the endogenous ligand for GHS-receptors (GHS-R), increases GH, ACTH, cortisol and glucose levels in humans. This study evaluated the GH, ACTH, cortisol and glucose-releasing effects of ghrelin in CD in comparison with GHRP-6. GHRH-induced GH release was also studied. Ten patients with CD (BMI 26.9+/-1.0 kg/m(2)) and ten controls (BMI 24.4+/-1.1 kg/m(2)) received ghrelin (1 microg/kg), GHRP-6 (1 microg/kg) and GHRH (100 microg) separately. GH, ACTH, cortisol and glucose levels were measured. In CD ghrelin-induced GH (microg/L; mean +/- SE) release (peak: 7.2+/-3.0) was higher than seen with GHRP-6 (2.7+/-1.0) and GHRH (0.7+/-0.2), but lower than in controls (ghrelin: 58.3+/-12.1; GHRP-6: 22.9+/-4.8; GHRH: 11.3+/-3.7). In controls ACTH (pg/mL) release after ghrelin (79.2+/-26.8) was higher than after GHRP-6 (23.6+/-5.7). In CD these responses (ghrelin: 192+/-43; GHRP-6: 185+/-56) were similar, and enhanced compared to controls. The same was observed with cortisol. Glucose levels failed to increase after ghrelin in CD, differently than in controls. Our data suggests that hypothalamic and pituitary pathways of GH release activated by ghrelin, GHRP-6 and GHRH are deranged in chronic hypercortisolism. The increased ACTH/cortisol responses to ghrelin and GHRP-6 in CD could be mediated by overexpression of GHS-R in ACTH-secreting adenomas. Hypercortisolism apparently impairs the ability of ghrelin to increase glucose levels. SN - 1386-341X UR - https://www.unboundmedicine.com/medline/citation/16832586/Decreased_GH_secretion_and_enhanced_ACTH_and_cortisol_release_after_ghrelin_administration_in_Cushing's_disease:_comparison_with_GH_releasing_peptide_6__GHRP_6__and_GHRH_ L2 - https://doi.org/10.1007/s11102-006-9149-8 DB - PRIME DP - Unbound Medicine ER -