What will be the effect of insulin on PFK-1?

This will ______________ glycolytic flux.

ATP is a substrate at low concentration, and a _______________ at high (accumulating) concentration.

Question

What will be the effect of insulin on PFK-1?

This will ______________ glycolytic flux.

ATP is a substrate at low concentration, and a _______________ at high (accumulating) concentration.

BlackTom AI · Accepted Answer

Insulin increases fructose‑2,6‑bisphosphate (F2,6BP), which allosterically activates PFK‑1 by increasing its affinity for fructose‑6‑phosphate (F6P); this raises glycolytic flux.

Relevant knowledge points:
- PFK‑1 (phosphofructokinase‑1) is the key regulatory, rate‑limiting enzyme of glycolysis converting F6P to F1,6BP.  
- Fructose‑2,6‑bisphosphate is a potent allosteric activator of PFK‑1 that decreases the Km for F6P (i.e., increases affinity).  
- Insulin promotes the dephosphorylated state of the bifunctional PFK‑2/FBPase‑2 enzyme (via protein phosphatase activity), shifting it toward its kinase activity that produces F2,6BP.  
- ATP serves as a substrate for PFK‑1 at low concentrations (donor of the phosphate), but at high (accumulating) concentrations ATP binds an allosteric inhibitory site and decreases PFK‑1 activity.

Step‑by‑step reasoning:
1. Insulin signaling activates phosphatases that dephosphorylate PFK‑2/FBPase‑2, favoring the kinase (PFK‑2) activity.  
2. Increased PFK‑2 activity raises intracellular F2,6BP levels.  
3. F2,6BP binds PFK‑1 allosterically, lowering its Km for F6P — i.e., increasing affinity — so PFK‑1 more readily converts F6P to F1,6BP.  
4. Increased PFK‑1 activity accelerates the glycolytic flux (more glucose carbons flow through glycolysis).  
5. ATP is required as a substrate for the PFK‑1 reaction when ATP is low, but when ATP accumulates it acts at a separate inhibitory site to signal energy sufficiency and slow glycolysis.

Why the correct option is correct:
- It explicitly states increased affinity for F6P (effect of F2,6BP), an increase in glycolytic flux (insulin's net effect), and that ATP is an inhibitor at high concentration.

Why other choices are incorrect:
- “Decrease affinity for F6P, decrease, activator” contradicts known activation by F2,6BP and insulin’s anabolic/glycolytic promotion.  
- “Increase affinity for F1,6BP, increase, inhibitor” misidentifies the ligand—PFK‑1 is regulated by F6P affinity and F2,6BP, not by increased affinity for its product F1,6BP.  
- “Increase affinity for F6P, increase, activator” is wrong about ATP: high ATP is inhibitory, not activating.

Final confirmation: the correct answer is “increase affinity for F6P, increase, inhibitor.”

What will be the effect of insulin on PFK-1? This will glycolytic flux. ATP is a substrate at low concentration, and a _ at high (accumulating) concentration.单项选择题

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What will be the effect of insulin on PFK-1? This will ______________ glycolytic flux. ATP is a substrate at low concentration, and a _______________ at high (accumulating) concentration.单项选择题