β Adrenergic receptors, in particular β2 subtype, are key regulators of glucose homeostasis. Previous studies showed that activation of hepatic and adipose tissue β adrenergic receptors mediates insulin desensitizing effects. On the contrary, activation of β adrenergic receptors in the skeletal muscle enhances glucose uptake. However, there is a lot of controversy regarding the metabolic effects of systemic administration of either β adrenergic receptor agonists or antagonists. β2 Agonists have been shown to substantially impair glucose homeostasis while improving it with long-term systemic administration. In the same context, acute and chronic systemic use of certain types of β blockers have been found to enhance insulin action. In this review article, we try to elaborate the underlying mechanisms that regulate glucose metabolism after acute and chronic systemic use of β adrenergic receptor agonists and antagonists in an attempt to answer the question "Do β adrenergic receptors induce or protect against insulin resistance?"