Hormonal Regulation—Effect of Insulin on Glucose Pathways Considering hepatic carbohydrate metabolism, which statement best describes insulin’s coordinated effects on gluconeogenesis and glycolysis?

Introduction / Context:
Insulin is an anabolic hormone secreted in response to elevated blood glucose. It promotes storage and utilization of glucose while suppressing endogenous glucose production. Distinguishing insulin’s effects on gluconeogenesis (making glucose) versus glycolysis (breaking down glucose) is fundamental to understanding fed-state metabolism.

Given Data / Assumptions:

• Tissue of interest: liver (primary regulator of blood glucose).
• Fed state: high insulin, low glucagon.
• Key regulatory enzymes affected by insulin signaling and phosphorylation states.

Concept / Approach:
Insulin activates glycolysis by increasing the activity of enzymes such as phosphofructokinase-1 (via increased fructose-2,6-bisphosphate through PFK-2), and pyruvate kinase. Simultaneously, insulin suppresses gluconeogenesis by downregulating key enzymes (PEP carboxykinase, fructose-1,6-bisphosphatase, glucose-6-phosphatase) at transcriptional and allosteric levels. Therefore, the correct combined effect is inhibition of gluconeogenesis and stimulation of glycolysis.

Step-by-Step Solution:

Verification / Alternative check:
Clinical observation: after carbohydrate ingestion, hepatic glucose output drops (less gluconeogenesis) while glucose utilization increases (more glycolysis and glycogenesis).

Why Other Options Are Wrong:

• A/B: insulin does not stimulate gluconeogenesis.
• C: insulin does not shut off glycolysis in liver.
• E: insulin profoundly affects both pathways.

Common Pitfalls:
Assuming insulin uniformly increases all glucose pathways; confusing liver regulation with muscle, which lacks glucose-6-phosphatase.

Final Answer:
Inhibits gluconeogenesis and stimulates glycolysis