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Neuroendocrine and metabolic effects of acute ghrelin administration in human obesity.
J Clin Endocrinol Metab. 2003 Nov; 88(11):5478-83.JC

Abstract

Ghrelin stimulates appetite and plays a role in the neuroendocrine response to energy balance variations. Ghrelin levels are inversely associated with body mass index (BMI), increased by fasting and decreased by food intake, glucose load, insulin, and somatostatin. Ghrelin levels are reduced in obesity, a condition of hyperinsulinism, reduced GH secretion, and hypothalamus-pituitary-adrenal axis hyperactivity. We studied the endocrine and metabolic response to acute ghrelin administration (1.0 microg/kg i.v.) in nine obese women [OB; BMI (mean +/- SD) 36.3 +/- 2.3 kg/m(2)] and seven normal women (NW; BMI 20.3 +/- 1.7 kg/m(2)). Basal ghrelin levels in NW were higher than in OB (P < 0.05). In NW, ghrelin increased (P < 0.05) GH, prolactin (PRL), ACTH, cortisol, and glucose levels but did not modify insulin. In OB, ghrelin increased (P < 0.01) GH, PRL, ACTH, and cortisol levels. The GH response to ghrelin in OB was 55% lower (P < 0.02) than in NW, whereas the PRL, ACTH, and cortisol responses were similar. In OB, ghrelin increased glucose and reduced insulin (P < 0.05). Thus, obesity shows remarkable reduction of the somatotroph responsiveness to ghrelin, suggesting that ghrelin hyposecretion unlikely explains the impairment of somatotroph function in obesity. On the other hand, in obesity ghrelin shows preserved influence on PRL, ACTH, and insulin secretion as well as in glucose levels.

Authors+Show Affiliations

Division of Endocrinology and Metabolism, Department of Internal Medicine, University of Turin, 10126 Turin, Italy.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)

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

Language

eng

PubMed ID

14602793

Citation

Tassone, F, et al. "Neuroendocrine and Metabolic Effects of Acute Ghrelin Administration in Human Obesity." The Journal of Clinical Endocrinology and Metabolism, vol. 88, no. 11, 2003, pp. 5478-83.
Tassone F, Broglio F, Destefanis S, et al. Neuroendocrine and metabolic effects of acute ghrelin administration in human obesity. J Clin Endocrinol Metab. 2003;88(11):5478-83.
Tassone, F., Broglio, F., Destefanis, S., Rovere, S., Benso, A., Gottero, C., Prodam, F., Rossetto, R., Gauna, C., van der Lely, A. J., Ghigo, E., & Maccario, M. (2003). Neuroendocrine and metabolic effects of acute ghrelin administration in human obesity. The Journal of Clinical Endocrinology and Metabolism, 88(11), 5478-83.
Tassone F, et al. Neuroendocrine and Metabolic Effects of Acute Ghrelin Administration in Human Obesity. J Clin Endocrinol Metab. 2003;88(11):5478-83. PubMed PMID: 14602793.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Neuroendocrine and metabolic effects of acute ghrelin administration in human obesity. AU - Tassone,F, AU - Broglio,F, AU - Destefanis,S, AU - Rovere,S, AU - Benso,A, AU - Gottero,C, AU - Prodam,F, AU - Rossetto,R, AU - Gauna,C, AU - van der Lely,A J, AU - Ghigo,E, AU - Maccario,M, PY - 2003/11/7/pubmed PY - 2003/12/10/medline PY - 2003/11/7/entrez SP - 5478 EP - 83 JF - The Journal of clinical endocrinology and metabolism JO - J. Clin. Endocrinol. Metab. VL - 88 IS - 11 N2 - Ghrelin stimulates appetite and plays a role in the neuroendocrine response to energy balance variations. Ghrelin levels are inversely associated with body mass index (BMI), increased by fasting and decreased by food intake, glucose load, insulin, and somatostatin. Ghrelin levels are reduced in obesity, a condition of hyperinsulinism, reduced GH secretion, and hypothalamus-pituitary-adrenal axis hyperactivity. We studied the endocrine and metabolic response to acute ghrelin administration (1.0 microg/kg i.v.) in nine obese women [OB; BMI (mean +/- SD) 36.3 +/- 2.3 kg/m(2)] and seven normal women (NW; BMI 20.3 +/- 1.7 kg/m(2)). Basal ghrelin levels in NW were higher than in OB (P < 0.05). In NW, ghrelin increased (P < 0.05) GH, prolactin (PRL), ACTH, cortisol, and glucose levels but did not modify insulin. In OB, ghrelin increased (P < 0.01) GH, PRL, ACTH, and cortisol levels. The GH response to ghrelin in OB was 55% lower (P < 0.02) than in NW, whereas the PRL, ACTH, and cortisol responses were similar. In OB, ghrelin increased glucose and reduced insulin (P < 0.05). Thus, obesity shows remarkable reduction of the somatotroph responsiveness to ghrelin, suggesting that ghrelin hyposecretion unlikely explains the impairment of somatotroph function in obesity. On the other hand, in obesity ghrelin shows preserved influence on PRL, ACTH, and insulin secretion as well as in glucose levels. SN - 0021-972X UR - https://www.unboundmedicine.com/medline/citation/14602793/Neuroendocrine_and_metabolic_effects_of_acute_ghrelin_administration_in_human_obesity_ L2 - https://academic.oup.com/jcem/article-lookup/doi/10.1210/jc.2003-030564 DB - PRIME DP - Unbound Medicine ER -