Discussion of all aspects of cellular structure, physiology and communication.
At what point is glucose either converted to fat or ATP and what causes it to go one way or another? I've found what I hope (and what my teacher has hinted) is the right pathway at http://www.genome.jp/kegg/pathway/map/map00620.html, but I'm not advanced enough to really understand what that means (I'm only finishing my first semester of AP Biology). I'm pretty sure it's the right pathway because it includes gycolysis and fatty acid biosynthesis, but I don't know how to tell where they branch off, and that still doesn't answer my question of what causes one of the branches to be taken.
Any help would be greatly appreciated.
I'm a second year med. student, and i was told by my organic chem. tutor that this site is a reliable source. At least i found it really helpful!
glucose -> pyruvate -> acetyl~CoA ->(by Acetyl CoA carboxylase) -> malonyl~CoA -> fatty acids
"As a biologist, I firmly believe that when you're dead, you're dead. Except for what you live behind in history. That's the only afterlife" - J. Craig Venter
Yes, but I need to know specifically why, like where the two pathways branch off. I found a biochem textbook yesterday that says that acetyl CoA is used for de novo fatty acid synthesis. So I think my question is, what decides whether acetyl CoA is used for fatty acid synthesis or goes into the citric acid cycle? Does it have something to do with too much glucose= too much pyruvate =too much acetyl CoA = some of it going for fatty acid synthesis instead of the citric acid cycle?
Thanks! This looks like it's going to be helpful.
From that website: "Glucose is converted to pyruvate (glycolysis), then to acetyl CoA which, when ATP is required, is oxidised by the citric acid cycle. If the glucose intake exceeds the body's energy needs (and after saturation of glycogen stores) the acetyl CoA can be used for fatty acid synthesis (in the liver) and storage as triglyceride in adipose tissue."
Is that the answer?
Sorry to be quadruple posting, but I just talked to my biology teacher and he says that I need to find what triggers acetyl CoA to become malonyl CoA. Is that something I could find online, or should I just go back to the biochemistry textbook?
you may be able to find it online, but your textbook is probably the best bet. It's not that hard, all you need is to look for regulation of acetyl-coa carboxylase.
Ok. I found that AMP regulates synthesis of fatty acids by regulating how much malonyl is available to be used, but could that be considered a "trigger" for whether acetyl coa becomes malonyl coa?
I am also confused about the role insulin plays in this entire process and about glycogen storage? Does the presence of elevated levels of insulin cause storage of glycogen and is acetyl coa involved directly in storing glycogen? And how relevant actually is glycogen to the question I'm trying to answer?
Thanks so much for your help.
Yes, that's the website I got it from. I just don't understand it very because, like I said, I've only had one semester of AP Biology. I understand most of it, just not about insulin, glycogen storage, and whether AMP is a trigger or not. You're saying all my questions are on there?
Edit: AP Biology is only one step above high school biology.
Last edited by Mithril on Sun Dec 14, 2008 4:03 pm, edited 1 time in total.
" AMP functions as an energy sensor and regulator of metabolism. When ATP production does not keep up with needs, a higher portion of a cell's adenine nucleotide pool is in the form of AMP. AMP promotes catabolic pathways that lead to synthesis of ATP, while inhibiting energy-utilizing synthetic pathways. For example, AMP regulates fatty acid synthesis and catabolism by controlling availability of malonyl-CoA."
"Regulation of Acetyl-CoA Carboxylase by local metabolites:
* Palmitoyl-CoA, the product of Fatty Acid Synthase, promotes the inactive conformation of Acetyl-CoA Carboxylase (diagram above), diminishing production of malonyl-CoA, the precursor of fatty acid synthesis. This is an example of feedback inhibition.
* Citrate allosterically activates Acetyl-CoA Carboxylase. Citrate concentration is high when there is adequate acetyl-CoA entering Krebs Cycle. Excess acetyl-CoA is then converted via malonyl-CoA to fatty acids for storage."
I think that's what you need.
As for insulin,
"A cyclic-AMP cascade, activated by the hormones glucagon and epinephrine when blood glucose is low, may also result in phosphorylation of Acetyl-CoA Carboxylase via cAMP-Dependent Protein Kinase. With Acetyl-CoA Carboxylase inhibited, acetyl-CoA remains available for synthesis of ketone bodies, the alternative metabolic fuel used when blood glucose is low. The antagonistic effect of insulin, produced when blood glucose is high, is attributed to activation of Protein Phosphatase."
You need to keep in mind what the effects of insulin are.
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