Human Anatomy, Physiology, and Medicine. Anything human!
I'm a dietetics student, and my course is really unclear about gluconeogenesis regulation, and exactly WHEN it happens.
What my coursebook teaches me is that glycogenolysis is the main purveyor of energy during physical exercise, and it is triggered by LOW INSULIN, HIGH GLUCAGON and HIGH ADRENALINE, which is exactly what happens when you start working out. So far so good.
But then they tell me that gluconeogenesis is triggered by LOW INSULIN, HIGH GLUCAGON and HIGH ADRENALINE, so: exactly the same conditions as above. And yet they keep saying throughout the chapter that gluconeogenesis SELDOM occurs during physical exertion itself, and that aminoacids are used only as a last resort, even though they specified a few pages before that the main substrate for GNG is alanine (followed by lactate and glycerol).
So there HAS to exist some factor that apparently delays GNG other than the aforementionned hormones, otherwise both metabolisms would start at the same time since they respond to the same hormonal changes. Right? But there is no mention of any such thing in my course.
I'm lost! If anyone could clear that up for me, I'd be really thankful.
I think the answer is in location. GNG takes place in liver where glucose is synthesised and transported to peripheral tissues where is it utilised. And it uses alanine as the solely amino acid, because it's freely exchangeable with pyruvate and lactate.
Cis or trans? That's what matters.
Thanks JackBean for these clues.
However I am still confused... If I understand correctly what you meant, the effects of GNG would be delayed because of the time it takes to transport glucose to peripheral tissues?
I wouldn't imagine that transport time to be that long (at least not the duration of a whole physical activity). I would imagine however that it would induce a delay of a couple of minutes...
Besides, I think the start of GNG should be determined by the time at which the liver starts using alanine/lactate to make glucose, not the time by which said glucose has reached the recipient cells. This is how I understand it, I may be wrong of course, and if I am, please help me understand!
But my question was about that exactly... I know that GNG happens, I just don't know when.
I don't see why not? As long as glucose levels are low... what would stop them from running?
The phosphorylase that starts glycogenolysis is inactivated by high levels of glucose, which quickly is not the case anymore as soon as physical activity starts, right? And it is also activated by calcium (through the phosphorylase kinase) due to muscle contraction.
Or am I mixing everything up?
Isn't gluconeogenesis SYNTHESIS of glucose, rather than breakdown of glycogen? I know that predators with almost no carb sources do that, but it seems that it would require pretty extreme conditions to kick in for human...
Yes, I'm not sure what your point is (?)
What makes you say that? I mean, how would you explain this assumption from a biochemical perspective?
Blood glucose has to remain stable at all costs, that's the number 1 priority for the body right (because of the brain, red cells and other glucose dependent tissues)? So as soon as glucose shows signs of decreasing, insuline drops and is replaced by glucagon+adrenaline released into the blood, which (according to all the textbooks I've come across) are triggers for both GNG and glycogenolysis. I mean, who's the boss? It's the hormones, right? So that's what I don't understand. The hormones responsible for GNG are present in the blood (since without them, glycogenolysis could not even happen) and yet we are told that GNG only takes place at a later stage. There's an information gap here, which is what I'd love anyone to clear up for me
And thanks for your attempt
JackBean I've just had a check at another textbook and you were right! Unlike what I first thought, glycolysis can't take place once glycogenolysis has started because the pyruvate kinase is inhibited by glucagon and adrenaline, so PEP can't turn into pyruvate anymore.
Which is only adding to my confusion...
I assumed that glycogen reserves would be enough except for extreme conditions, and that is sort of true...
Ths has a decent overview -
Thanks Darby, but the article is about renal gluconeogenesis, which starts only in prolonged fasting conditions, unlike liver GNG.
Yes it is true that glycogen reserves would usually be enough, but that doesn't mean that GNG does not take place all the same, apparently both metabolisms can occur at the same time, although one might be quicker than the other. When exactly when GNG starts and why the delay, compared with glycogenolysis...
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