Step 1: Evaluate each statement against the physiology of glucose production. Gluconeogenesis is a hepatic and renal process that defends the blood glucose level during fasting.
Step 2: Muscle cannot carry it out to completion because it has no glucose-6-phosphatase, so the muscle statement fails. Fructose 2,6-bisphosphate is the master activator of glycolysis and a brake on gluconeogenesis, so that statement is also false.
Step 3: Acetyl CoA, which rises in fasting as fat is oxidised, is an allosteric activator of pyruvate carboxylase and therefore stimulates gluconeogenesis; the claim that it inhibits the pathway is incorrect.
Step 4: The remaining choice is sound: in the post-absorptive (overnight fasting) state, gluconeogenesis together with glycogenolysis keeps blood glucose steady, and once glycogen is exhausted gluconeogenesis carries the entire load.
\[\boxed{\text{It maintains blood glucose during the normal overnight fast}}\]