Beta-adrenergic agonism does not impair the GH response to acylated ghrelin in humans
Autor: | Andrea Benso, Fabio Broglio, V. Ramella Gigliardi, D H St Pierre, Elena Gramaglia, Fabrizio Riganti, Flavia Prodam, Ilaria Olivetti, Barbara Lucatello, Ezio Ghigo |
---|---|
Rok vydání: | 2008 |
Předmět: |
Adult
Male medicine.medical_specialty Somatotropic cell Adrenergic receptor Endocrinology Diabetes and Metabolism Acylation Adrenergic Endocrinology Internal medicine medicine Humans Secretion Albuterol Infusions Intravenous Chemistry Human Growth Hormone Adrenergic beta-Agonists Growth hormone secretion Ghrelin Somatostatin Salbutamol medicine.drug |
Zdroj: | Clinical endocrinology. 71(2) |
ISSN: | 1365-2265 |
Popis: | Summary Background Acylated ghrelin (AG) is a physiological GH secretion amplifier, in part stimulating GHRH neurones and antagonizing somatostatin activity. In humans, AG is one of the most potent pharmacological stimuli of GH secretion and, unlike GHRH, is refractory to the inhibitory effect of glucose, free fatty acids (FFA) and somatostatin. Somatotroph secretion is also profoundly modulated by the adrenergic system. Indeed, beta-adrenergic agonists abolish spontaneous and GHRH-stimulated GH secretion. Based on these data, the aim of the present study was to investigate the effects of beta adrenergic agonism on the GH response to AG. Subjects and measurements Six young healthy male volunteers underwent: (a) acute AG intravenous (iv) administration (1·0 µg/kg); (b) salbutamol infusion (SLB; 0·06 µg/kg/min iv); (c) AG + SLB; and (d) saline infusion. In all sessions GH levels were assayed every 15 min from time –30 to +210 min. Results SLB induced a significant (P |
Databáze: | OpenAIRE |
Externí odkaz: |