Interestingly, both beta-agonists and antagonists are implicated in causing diabetes through different mechanisms. Increased beta-receptor stimulation has been shown to increase plasma glucose via increase in glycogenolysis and lipolysis, despite increased insulin secretion (46). Beta-agonist's diabetogenic potential is dose-dependent and more pronounced with intravenous and oral route than subcutaneous route (47). There are case reports of diabetic ketoacidosis after the infusion of beta-2 agonists (48). Multiple mechanisms have been proposed for this diabetogenic potential of beta-agonists: increase in hepatic glucose production, increase in peripheral insulin resistance and increase in plasma glucagons following beta-2 agonists and increase in lipolysis (45).
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