**Core Concept**
The metabolic effects of sympathomimetics are primarily mediated through the activation of adrenergic receptors, specifically beta-1 (β1) and beta-2 (β2) receptors, which are part of the sympathetic nervous system. This activation leads to increased glycogenolysis, gluconeogenesis, and lipolysis, resulting in increased glucose and lipid metabolism.

**Why the Correct Answer is Right**
The correct answer is mediated by the activation of β1 and β2 receptors. β1 receptors are primarily found in the heart, where they increase heart rate and contractility. β2 receptors are found in adipose tissue, liver, and skeletal muscle, where they stimulate lipolysis, glycogenolysis, and gluconeogenesis. This results in increased glucose production and release, as well as increased lipid metabolism.

**Why Each Wrong Option is Incorrect**
**Option A:** This option is incorrect because it does not specify the receptor subtype responsible for the metabolic effects of sympathomimetics.
**Option B:** This option is incorrect because it does not accurately describe the mechanisms of action of sympathomimetics on glucose and lipid metabolism.
**Option C:** This option is incorrect because it does not specify the receptor subtype responsible for the metabolic effects of sympathomimetics.

**Clinical Pearl / High-Yield Fact**
It's essential to remember that sympathomimetics, such as epinephrine and norepinephrine, have both α and β adrenergic effects. The α effects are primarily vasoconstrictive, while the β effects are primarily metabolic. Understanding the specific receptor subtypes and their effects is crucial in managing patients with sympathomimetic-induced hypermetabolism.

**Correct Answer:** C. Activation of β1 and β2 receptors.