Hello, I have an essay question which is "Discuss hormonal and non-hormonal mechanisms for the control of blood glucose levels". I'm not sure if this is the right place to post this but if someone could let me know that would be great! 
I have a few questions about this essay:
- What are "non-hormonal" mechanisms of control of glucose levels?
- What are the acute and chronic effects or glucagon and insulin?
- What role does adipose tissue play in glucose regulation?
- With regards to the glucose-fatty acid cycle/Randle cycle, does fatty acid oxidation stop glycogen synthesis in skeletal muscle? If so, how does this help spare glucose for the brain (at the moment my understanding is that the point of the glucose-fatty acid cycle is to allow the glucose-sparing effect)?
- Also, I am a little confused as I read this on Wikipedia:
"The glucose fatty acid cycle is also observed in the fed state after a high-fat meal or during exercise. This is when plasma concentrations of fatty acids or ketone bodies are increased. The glucose that is not oxidized is then rerouted to glycogen. This rerouting to glycogen explains the rapid resynthesis of muscle glycogen after exercise as well as the increased glycogen content in muscles found in starvation or diabetes. This mechanism replenishes the intermediates of the citric acid cycle."
- First of all, how can someone be in the fed state if they are exercising?
- Why would ketone body concentration be high in the fed state? Is it because with a high fat meal glycogen stores are likely to be depleted quickly and this is then followed by lipolysis to form free fatty acids (which could be used by the heart and skeletal muscle directly) which are then oxidised to produce acetyl CoA which is used to form ketone bodies? If this is the case, I am wondering why in the next line ("glucose that is not oxidised...") the paragraph talks about production of glycogen- if ketones are being produced why would glycogen be being produced?
- Fatty acid oxidation is supposed to prevent synthesis of glycogen in skeletal muscle (taken from a Textbook of Biochemistry by Devlin), is this only the case in the fasted state and therefore the paragraph above is correct because it is stating the glycogen synthesis occurs in the fed state?
-Finally, slightly random, but can one develop ketoacidosis if they are not diabetic- I have read various things online that seem to contradict each including cases of non-diabetic patients developing ketoacidosis?
Apologies for all of the jumbled questions. As you can see I am quite confused at the moment and would really appreciate any help as I am revising for a first year resit!
I have a few questions about this essay:
- What are "non-hormonal" mechanisms of control of glucose levels?
- What are the acute and chronic effects or glucagon and insulin?
- What role does adipose tissue play in glucose regulation?
- With regards to the glucose-fatty acid cycle/Randle cycle, does fatty acid oxidation stop glycogen synthesis in skeletal muscle? If so, how does this help spare glucose for the brain (at the moment my understanding is that the point of the glucose-fatty acid cycle is to allow the glucose-sparing effect)?
- Also, I am a little confused as I read this on Wikipedia:
"The glucose fatty acid cycle is also observed in the fed state after a high-fat meal or during exercise. This is when plasma concentrations of fatty acids or ketone bodies are increased. The glucose that is not oxidized is then rerouted to glycogen. This rerouting to glycogen explains the rapid resynthesis of muscle glycogen after exercise as well as the increased glycogen content in muscles found in starvation or diabetes. This mechanism replenishes the intermediates of the citric acid cycle."
- First of all, how can someone be in the fed state if they are exercising?
- Why would ketone body concentration be high in the fed state? Is it because with a high fat meal glycogen stores are likely to be depleted quickly and this is then followed by lipolysis to form free fatty acids (which could be used by the heart and skeletal muscle directly) which are then oxidised to produce acetyl CoA which is used to form ketone bodies? If this is the case, I am wondering why in the next line ("glucose that is not oxidised...") the paragraph talks about production of glycogen- if ketones are being produced why would glycogen be being produced?
- Fatty acid oxidation is supposed to prevent synthesis of glycogen in skeletal muscle (taken from a Textbook of Biochemistry by Devlin), is this only the case in the fasted state and therefore the paragraph above is correct because it is stating the glycogen synthesis occurs in the fed state?
-Finally, slightly random, but can one develop ketoacidosis if they are not diabetic- I have read various things online that seem to contradict each including cases of non-diabetic patients developing ketoacidosis?
Apologies for all of the jumbled questions. As you can see I am quite confused at the moment and would really appreciate any help as I am revising for a first year resit!
