Gluconeogenesis

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Tokspor

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I had a practice passage about gluconeogenesis and had some confusion with one of the questions.

The information in the passage states that in "hepatic forms" of certain diseases classified as glycogenoses, there is "an inherited deficiency of hepatic enzymes responsible for the breakdown of glycogen" This results in an "excess storage of glycogen in the liver."

Also, in "myopathic forms" of glycogenoses, a "deficiency in the enzymes of glycolysis in striated muscle results in...impaired ability to produce ATP."

One of the questions then asks which of the following is likely to result from this hepatic form of glycogenoses but not myopathic forms.

A. Increased extracellular glycogen concentration
B. Decreased blood glucose concentration
C. Decreased gluconeogenesis
D. Decreased O2 consumption

The correct answer is B.

The text's reasoning for C being wrong is that "an inability to breakdown glycogen would starve the body of glucose, leading to an increase in gluconeogenesis." But this should happen in hepatic forms since a build-up of glycogen indicates decreased gluconeogenesis, right? And it shouldn't happen in myopathic forms because we're told it's the glycolysis step, not the breakdown of glycogen, which is impaired here. So shouldn't C be correct as well?

Any thoughts on why B is a better answer than C?

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You're correct... except your forgetting about just what's happening with this disease. Under normal conditions, when there's excess energy, glycogen will be created in the liver... as you know. The disease won't allow for glycogen to break down in order to increase blood glucose levels... so in turn there will be an increase in gluconeogenesis to sustain glucose concentration.
 
I had a practice passage about gluconeogenesis and had some confusion with one of the questions.

The information in the passage states that in "hepatic forms" of certain diseases classified as glycogenoses, there is "an inherited deficiency of hepatic enzymes responsible for the breakdown of glycogen" This results in an "excess storage of glycogen in the liver."

Also, in "myopathic forms" of glycogenoses, a "deficiency in the enzymes of glycolysis in striated muscle results in...impaired ability to produce ATP."

One of the questions then asks which of the following is likely to result from this hepatic form of glycogenoses but not myopathic forms.

A. Increased extracellular glycogen concentration
B. Decreased blood glucose concentration
C. Decreased gluconeogenesis
D. Decreased O2 consumption

The correct answer is B.

The text's reasoning for C being wrong is that "an inability to breakdown glycogen would starve the body of glucose, leading to an increase in gluconeogenesis." But this should happen in hepatic forms since a build-up of glycogen indicates decreased gluconeogenesis, right? And it shouldn't happen in myopathic forms because we're told it's the glycolysis step, not the breakdown of glycogen, which is impaired here. So shouldn't C be correct as well?

Any thoughts on why B is a better answer than C?

C is not correct because the body needs glucose. Think about it-you have these deficient hepatic enzymes that are unable to break down glycogen into glucose, and then on top of that the liver is going to shut down gluconeogenesis as well!? Now, that would be one evil liver :laugh: The liver needs to compensate for that deficiency, and thus, would up its gluconeogenesis.
 
Thanks for your responses. I was not familiar enough with the terminology here--I thought gluconeogenesis was any process which creates glucose, even the phosphorylation of glycogen to glucose. It should have been clear to me that they are different pathways to glucose.

So C would be incorrect because gluconeogenesis increases in the liver due to a lack of glucose. And could we also reason that there would be a decrease in gluconeogenesis in the muscle since there is a build-up of glucose there?

Also, as for B being correct, since gluconeogenesis is expected to proceed in the liver, yet there is still expected to be a decrease in blood glucose, does this mean gluconeogenesis is not as efficient a means of obtaining glucose as the phosphorylation of glycogen?
 
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Gluconeogenesis is the production of glucose from non-carbohydrates. Glycogen is a carbohydrate.

Gluconeogenesis only takes place in the liver. Muscle cells can only absorb glucose and break down their own glycogen.

It's a matter of steps. Gluconeogenesis is efficient. It's just not the prefered way becasue there's no reason to start breaking down amino acids, and other molecules, to bring up the glucose concentration if there's glycogen present. In a sense, you could say it's not as efficient because it's further down the ladder, but it does efficiently synthesize glucose. In the question, you are only supposed to answer what the result of impaird glycogen break down is. The result of that would be decreased glucose concentration. Then the result of the decreased glucose concentration is an increase in gluconeogenesis. The result of increased gluconeogenesis is an increase in glucose concentration. You could go on and on with homeostatic regulation to the point of death, but the question is only asking what the result of glycogenolysis is.
 
When you're talking about increased glucose concentration, are you talking about it being in the blood or just about anywhere in the body?
 
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