, Volume 33, Issue 6, pp 363-367
Date: 27 Mar 2014

The metabolic response to the activation of the β- adrenergic receptor by salbutamol is amplified by acylated ghrelin

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Background: It is well recognized that β-adrenergic receptors mediate important endocrine and metabolic actions. In fact, β-adrenergic receptor activation negatively influences GH secretion while exerting relevant metabolic actions such as the stimulation of insulin secretion, glycogenosis, and lipolysis. Aim: We have already shown that the activation of the GH secretagogue receptor (GHS-R)-1a by acylated ghrelin (AG) counteracts the inhibitory effect of salbutamol (SALB), a β2-adrenergic agonist, on GH release. The aim of the present study in humans was to clarify whether the metabolic response to SALB is affected by the infusion of AG, also known to exert significant metabolic actions. Methods: Six healthy young male volunteers underwent the following testing sessions in random order at least 5 days apart: a) SALB (0.06 μg/kg/min iv from 0 to 60 min) alone; b) SALB in combination with AG (1.0 μg/kg/min iv from −60 to 60 min); c) isotonic saline. Insulin, glucose, and free fatty acids (FFA) levels were evaluated every 15 min. Results: As expected, with respect to saline, SALB administration tended to increase both insulin secretion [Δ area under the curve (ΔAUC): 0.16±0.09 vs 0.003±0.077 × 103 μU/ml/min; p>0.05] and FFA levels (ΔAUC: 8.0±7.3 vs ∼-4.0±4.0 mEq/l/min; p>0.05), while glucose levels did not change. The metabolic response to SALB was significantly modified under the exposure of AG. In fact, under AG infusion, SALB elicited a more marked increase of FFA (ΔAUC: 22.3±3.2 vs 8.0±7.3 mEq/l/min; p<0.05) as well as a slight elevation in insulin (ΔAUC: 0.37±0.11 vs 0.16±0.09 × 103 μU/ml/min; p>0.05). Under AG, the baseline glucose levels were more elevated but, again, in combination with AG, SALB did not significantly modify glucose levels. Conclusions: β-adrenergic receptors and AG are likely to interact at the metabolic level. In humans, the lypolitic response to a β2-adrenergic agonist such as SALB is amplified by AG. Meanwhile, during the co-treatment, the marginal insulinotropic effect was not associated with an increase in glycemia.

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