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

Abstract

Beta-adrenergic receptors and AG are likely to interact at the metabolic level. In humans, the lypolitic response to a beta2-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.

In Reply to “Thyrotoxic Periodic Paralysis, β2-Adrenergic Bronchodilator, and Insulin—An Interesting Interplay”

“…b 2 -Agonist is known to stimulate insulin secretion and may accordingly predispose TPP patients to acute hypokalemia. 3 On the other hand, it should be noted that nearly 80% of TPP attacks cannot be triggered by iatrogenic hyperinsulinemia after carbohydrate load. 4 The pathogenesis of TPP is clearly multifactorial and includes environmental stimulations (e.g., vigorous exercise, carbohydrate meal, etc.…”