Fructose 1,6-bisphosphate accumulation would have what regulatory effect on carbohydrate metabolism pathways operating in the cytosol?

Introduction / Context:
Reciprocal regulation prevents futile cycles between glycolysis and gluconeogenesis. Fructose 1,6-bisphosphate (F1,6BP) is a central allosteric signal that coordinates pathway flux, especially in the liver.

Given Data / Assumptions:

• Metabolite of interest: F1,6BP.
• Target enzymes: pyruvate kinase (glycolysis) and fructose 1,6-bisphosphatase (FBPase-1; gluconeogenesis).
• Physiological context: cytosolic carbohydrate metabolism.

Concept / Approach:
F1,6BP exerts feed-forward activation of pyruvate kinase, enhancing glycolytic flux. Conversely, high F1,6BP indicates that FBPase-1 should be less active to avoid simultaneous opposing flux, effectively suppressing gluconeogenesis (while phosphofructokinase-1 is upstream regulated by ATP/citrate/AMP).

Step-by-Step Solution:
1) Identify regulatory node: F1,6BP positively regulates pyruvate kinase → stimulates glycolysis.2) Consider gluconeogenesis: elevated F1,6BP reduces the need for FBPase-1 activity (reciprocal control), limiting gluconeogenic flux.3) Outcome: glycolysis stimulated; gluconeogenesis inhibited.

Verification / Alternative check:
Liver pyruvate kinase is activated by F1,6BP (feed-forward). Meanwhile, gluconeogenesis is favored when F2,6BP is low and ATP/acetyl-CoA are high; high F1,6BP signals glycolytic progress and opposes gluconeogenic pull.

Why Other Options Are Wrong:
Simultaneous inhibition or stimulation of both pathways violates reciprocal regulation.Inhibit glycolysis and stimulate gluconeogenesis contradicts known feed-forward activation of pyruvate kinase by F1,6BP.

Common Pitfalls:
Confusing F1,6BP with F2,6BP (a powerful modulator of PFK-1/FBPase-1). Both are regulators but have distinct targets and effects.

Final Answer:
Stimulate glycolysis and inhibit gluconeogenesis