Glycolysis regulation by F2,6BP

[MudPhud20XX]

So this is one of the questions from Kaplan asking:

A congenital deficiency in the enzyme phosphofructokinase-2 (PFK-2) would most likely impair which of the following processes?

The correct answer: Regulation of phosphofructokinase-1 (PFK-1) by insulin
(Other answer choices did not make any sense.)

I checked both FA and Kaplan biochem and PFK-1 is not regulated by insulin, so I don't get this.

If there is a defect in the enzyme PFK-2, it won't make F2,6BP that can stimulate PFK-1 to convert F6P to F1,6BP. That's really the only thing I can think of as an outcome of the PFK-2 defect.

Can anyone help me? Many thanks in advance.

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[ulikedaggers]

You answered your own question. Insulin activates protein phosphatase 1, which dephosphorylates the bifunctional enzyme (PFK-2 + F2,6BPase) in the liver only. If there's a defect in PFK-2, it won't respond to dephosphorylation (in the liver only) and the liver will start acting like all the other tissues and make glycogen instead of fat, which would be bad since the liver has a limited ability to store glycogen and eventually hyperglycemia would result.

 

[Myxedema]

 

[Myxedema]

I've made this image before, I've added the last part to answer your question. Hope this helps.