Hormone signaling cascades — adrenaline versus thyroxine A signaling cascade triggered by adrenaline (epinephrine) or by thyroxine (T4) has which reliably true feature?

Introduction:
Adrenaline and thyroxine signal through different receptor classes: adrenaline acts via GPCRs at the plasma membrane; thyroxine (T4) is a lipophilic hormone that crosses membranes and binds nuclear receptors. Despite this difference, both ultimately modulate enzymatic activities to produce physiological effects.

Given Data / Assumptions:

• Adrenaline → GPCR → G protein → second messengers → kinases (rapid enzymatic cascades).
• Thyroxine → nuclear receptor → gene transcription → altered enzyme expression (slower genomic effects).
• Both pathways culminate in enzyme activation or changes in enzyme levels.

Concept / Approach:

Evaluate each option against both hormones. A and B are true for adrenaline but not for thyroxine (which uses intracellular receptors and does not require G proteins). The common, reliable statement is that signaling causes activation or regulation of enzymes necessary for the cellular response, making Option C correct.

Step-by-Step Solution:

Verification / Alternative check:

Physiology shows adrenaline rapidly activates glycogen phosphorylase (via PKA), while thyroid hormones increase basal metabolic rate by upregulating mitochondrial and metabolic enzymes.

Why Other Options Are Wrong:

Option A: Thyroid hormone response does not begin at a surface receptor.

Option B: Thyroxine does not require heterotrimeric G proteins.

Option D: Since A and B fail for thyroxine, “all of the above” is incorrect.

Option E: Contradicts abundant data showing enzyme activation/regulation by both hormones.

Common Pitfalls:

Assuming all hormones use GPCRs or that genomic signaling lacks enzymatic consequences.

Final Answer:

It results in activation of a sequence of enzymes required for the cell’s effect