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Ghrelin does not mediate the somatotroph and corticotroph responses to the stimulatory effect of glucagon or insulin-induced hypoglycaemia in humans.
Clin Endocrinol (Oxf). 2004 Jun; 60(6):699-704.CE

Abstract

OBJECTIVE

Acylated ghrelin, a gastric peptide, possesses a potent GH- but also significant ACTH/cortisol-releasing activity mediated by the activation of GH secretagogue receptors (GHS-R) at the hypothalamus-pituitary level. The physiological role of ghrelin in the control of somatotroph and corticotroph function is, however, largely unclear. Glucagon is known to induce a clear increase of GH, ACTH and cortisol levels in humans, at least after intramuscular administration. In fact, glucagon is considered to be a classical alternative to insulin-induced hypoglycaemia (ITT) for the combined evaluation of the function of GH and the hypothalamus-pituitary-adrenal (HPA) axis. We aimed to clarify whether ghrelin mediate the GH and corticotroph responses to intramuscular glucagon or ITT, which has recently been reported able to induce a surprising ghrelin decrease.

SUBJECTS

To this aim we enrolled six normal young male subjects [age (mean +/- SD): 29.0 +/- 8.0 years, body mass index (BMI) 21.9 +/- 2.5 kg/m(2)].

DESIGN AND MEASUREMENTS

In all the subjects we studied ghrelin, GH, ACTH, cortisol and glucose levels after glucagon (GLU; 0.017 mg/kg intramuscularly), ITT (0.1 IU/kg insulin intravenously) or saline administration.

RESULTS

Saline infusion was not followed by any significant variation in ghrelin, GH and glucose levels while ACTH and cortisol showed the expected spontaneous morning trend toward a decrease. GLU administration increased (P < 0.01) circulating GH, ACTH and cortisol as well as insulin and glucose levels. ITT induced an obvious increase (P < 0.01) of GH, ACTH and cortisol levels. The ITT-induced increases in GH and ACTH, but not cortisol, levels were higher (P < 0.01) than those after GLU. Circulating ghrelin levels were not modified by GLU. On the other hand, ghrelin levels underwent a transient reduction (P < 0.01) after insulin-induced hypoglycaemia.

CONCLUSIONS

Ghrelin does not mediate the GH and ACTH responses to glucagon or to the ITT. In fact, ghrelin levels are not modified at all by glucagon and transiently decrease during the ITT. These findings support the assumption that ghrelin does not play a major role in the physiological control of somatotroph and corticotroph function.

Authors+Show Affiliations

Division of Endocrinology and Metabolism, Department of Internal Medicine, Erasmus University of Rotterdam, Rotterdam, The Netherlands.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

15163333

Citation

Broglio, Fabio, et al. "Ghrelin Does Not Mediate the Somatotroph and Corticotroph Responses to the Stimulatory Effect of Glucagon or Insulin-induced Hypoglycaemia in Humans." Clinical Endocrinology, vol. 60, no. 6, 2004, pp. 699-704.
Broglio F, Prodam F, Gottero C, et al. Ghrelin does not mediate the somatotroph and corticotroph responses to the stimulatory effect of glucagon or insulin-induced hypoglycaemia in humans. Clin Endocrinol (Oxf). 2004;60(6):699-704.
Broglio, F., Prodam, F., Gottero, C., Destefanis, S., Me, E., Riganti, F., Giordano, R., Picu, A., Balbo, M., Van der Lely, A. J., Ghigo, E., & Arvat, E. (2004). Ghrelin does not mediate the somatotroph and corticotroph responses to the stimulatory effect of glucagon or insulin-induced hypoglycaemia in humans. Clinical Endocrinology, 60(6), 699-704.
Broglio F, et al. Ghrelin Does Not Mediate the Somatotroph and Corticotroph Responses to the Stimulatory Effect of Glucagon or Insulin-induced Hypoglycaemia in Humans. Clin Endocrinol (Oxf). 2004;60(6):699-704. PubMed PMID: 15163333.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Ghrelin does not mediate the somatotroph and corticotroph responses to the stimulatory effect of glucagon or insulin-induced hypoglycaemia in humans. AU - Broglio,Fabio, AU - Prodam,Flavia, AU - Gottero,Cristina, AU - Destefanis,Silvia, AU - Me,Elisa, AU - Riganti,Fabrizio, AU - Giordano,Roberta, AU - Picu,Andreea, AU - Balbo,Marcella, AU - Van der Lely,Aart Jan, AU - Ghigo,Ezio, AU - Arvat,Emanuela, PY - 2004/5/28/pubmed PY - 2004/8/21/medline PY - 2004/5/28/entrez SP - 699 EP - 704 JF - Clinical endocrinology JO - Clin. Endocrinol. (Oxf) VL - 60 IS - 6 N2 - OBJECTIVE: Acylated ghrelin, a gastric peptide, possesses a potent GH- but also significant ACTH/cortisol-releasing activity mediated by the activation of GH secretagogue receptors (GHS-R) at the hypothalamus-pituitary level. The physiological role of ghrelin in the control of somatotroph and corticotroph function is, however, largely unclear. Glucagon is known to induce a clear increase of GH, ACTH and cortisol levels in humans, at least after intramuscular administration. In fact, glucagon is considered to be a classical alternative to insulin-induced hypoglycaemia (ITT) for the combined evaluation of the function of GH and the hypothalamus-pituitary-adrenal (HPA) axis. We aimed to clarify whether ghrelin mediate the GH and corticotroph responses to intramuscular glucagon or ITT, which has recently been reported able to induce a surprising ghrelin decrease. SUBJECTS: To this aim we enrolled six normal young male subjects [age (mean +/- SD): 29.0 +/- 8.0 years, body mass index (BMI) 21.9 +/- 2.5 kg/m(2)]. DESIGN AND MEASUREMENTS: In all the subjects we studied ghrelin, GH, ACTH, cortisol and glucose levels after glucagon (GLU; 0.017 mg/kg intramuscularly), ITT (0.1 IU/kg insulin intravenously) or saline administration. RESULTS: Saline infusion was not followed by any significant variation in ghrelin, GH and glucose levels while ACTH and cortisol showed the expected spontaneous morning trend toward a decrease. GLU administration increased (P < 0.01) circulating GH, ACTH and cortisol as well as insulin and glucose levels. ITT induced an obvious increase (P < 0.01) of GH, ACTH and cortisol levels. The ITT-induced increases in GH and ACTH, but not cortisol, levels were higher (P < 0.01) than those after GLU. Circulating ghrelin levels were not modified by GLU. On the other hand, ghrelin levels underwent a transient reduction (P < 0.01) after insulin-induced hypoglycaemia. CONCLUSIONS: Ghrelin does not mediate the GH and ACTH responses to glucagon or to the ITT. In fact, ghrelin levels are not modified at all by glucagon and transiently decrease during the ITT. These findings support the assumption that ghrelin does not play a major role in the physiological control of somatotroph and corticotroph function. SN - 0300-0664 UR - https://www.unboundmedicine.com/medline/citation/15163333/Ghrelin_does_not_mediate_the_somatotroph_and_corticotroph_responses_to_the_stimulatory_effect_of_glucagon_or_insulin_induced_hypoglycaemia_in_humans_ L2 - https://onlinelibrary.wiley.com/resolve/openurl?genre=article&amp;sid=nlm:pubmed&amp;issn=0300-0664&amp;date=2004&amp;volume=60&amp;issue=6&amp;spage=699 DB - PRIME DP - Unbound Medicine ER -