Counter-Regulatory Hormones—Actions of Glucagon and Epinephrine In hepatocytes during fasting or acute stress, which combined effect on carbohydrate pathways is produced by glucagon and epinephrine?

Introduction / Context:
Glucagon (from pancreatic α-cells) and epinephrine (adrenal medulla) are counter-regulatory to insulin. They mobilize fuel, maintain blood glucose, and prepare tissues for acute energy demands. Correctly identifying their push–pull effects on hepatic gluconeogenesis and glycolysis is pivotal for understanding fasting physiology and stress responses.

Given Data / Assumptions:

• Target tissue: liver.
• Signal pathways: cAMP/PKA and Ca2+ in some contexts.
• Key regulatory nodes: PFK-1/FBPase-1 via F2,6BP, pyruvate kinase phosphorylation, PEPCK expression.

Concept / Approach:
Glucagon/epinephrine lower fructose-2,6-bisphosphate via PKA-mediated phosphorylation of PFK-2/FBPase-2, decreasing PFK-1 (glycolysis) and increasing FBPase-1 (gluconeogenesis). They also inhibit hepatic pyruvate kinase and induce PEPCK/G6Pase expression, collectively suppressing glycolysis while promoting gluconeogenesis to export glucose.

Step-by-Step Solution:

Verification / Alternative check:
Physiology: fasting increases hepatic glucose output; catecholamines augment this during stress—consistent with the selected option.

Why Other Options Are Wrong:

• A/D: opposite of the biologic goal to raise blood glucose.
• B: simultaneous stimulation wastes substrate; not the physiologic response.
• E: strong hormonal signals clearly shift fluxes.

Common Pitfalls:
Projecting muscle regulation onto liver; in muscle, epinephrine increases glycolysis for local ATP but liver response is different.

Final Answer:
Stimulate gluconeogenesis and inhibit glycolysis