Term
|
Definition
| the formation of glucose from multiple different non-carbohydrate precursors |
|
|
Term
| Describe an overview of the pathway by which lactate is converted back to glucose |
|
Definition
1. Lactate is made in abundance during times of exercise
2. Lactate is released into the blood as blood lactate
3. The liver takes it up and burns ATP to synthesize glucose
4. Glucose is released back into the bloodstream for muscles to use and store as glycogen |
|
|
Term
| What precursor molecules can glucose be synthesized from? |
|
Definition
1. lactate and pyruvate
2. amino acids
3. propionate
4. glycerol |
|
|
Term
| What conditions facilitate gluconeogenesis? |
|
Definition
1. Glycogen stores are depleted
2. Tissues are starved of O2 (leads to excessive amounts of precursor molecules in the blood)
3. Amino acids or fats are catabolized for energy |
|
|
Term
| What precursors lead to pyruvate? which lead to oxaloacetate? which lead directly to triose phosphates? |
|
Definition
Lactate and amino acids go to pyruvate
Amino acids (other ones) and propionate go to oxaloacetate
Glycerol does directly to triose phosphates
After this:
Pyruvate --> oxaloacetate --> Triose phosphates --> glucose. |
|
|
Term
| what are the three irreversible steps in gluconeogenesis and what enzymes control them? |
|
Definition
1. Pyruvate --> oxaloacetate --> PEP
Step1 = pyruvate carboxylase
Step2 = PEP carboxykinase
2. F1,6B --> Fructose 6-Phosphate by fructose 1,6-biphosphatase
3. Glucose 6-Phosphate --> Glucose by glucose 6 phosphatase |
|
|
Term
| Describe the regulation of Fructose 1,6 Biphosphatase |
|
Definition
1. Elevated levels of fructose 2,6 biphosphate keep it down
2. Release of glucagon from the pancreas in response to low blood sugar will increase it (via same pathway as glycolysis, it activates adenyl cyclase, which increases protein kinase A, which phosphorylates PRK-2 which stops F2,6B production)
3. Decreased Insulin activity |
|
|
Term
| Why are muscles incapable of performing gluconeogenesis? |
|
Definition
| Muscles lack PEP carboxykinase, so they must send precursors over to the liver for these steps |
|
|
Term
| Why is glucose 6-phosphatase role in gluconeogenesis? |
|
Definition
| Removal of phosphate from glucose 6-phophate allowing it to be released back into the bloodstream by glucose transporters |
|
|
Term
| Where does gluconeogenesis take place and why |
|
Definition
Mostly liver, some kidney as well
These are the only places that have all the essential enzymes |
|
|
Term
| Describe the Cori cycle (starting with glycolysis) and the cost/benefits in terms of ATP |
|
Definition
1. Glycolysis in red blood cells makes lactate
2. Lactate is pumped into the bloodstream
3. Lactate is taken up by the liver
4. Gluconeogenesis turns lactate back into glucose
5. Glucose is released into the blood stream
6. Glucose is taken back up by RBC's and used for glycolysis
It costs 6 ATP to perform gluconeogensis, and only 2 ATP are yielded from the glycolysis in RBC. So it is a very inefficient system, but its the only system we have |
|
|
Term
| Describe the alanine cycle, where it occurs, and its relative efficiency to the Cori Cycle |
|
Definition
1. Proteins and pyruvate are broken down into alanine
2. Alaine is released and taken up by the liver
3. Alanine under goes gluconeogenesis (and a release of a nitrogen allows ureogenesis to occur alongside this)
4. Glucose is released and taken back up by muscles
5. Glycolysis can continue
Alanine cycle occurs in muscle with partial O2 deprivation
It costs 10 ATP and can produce 5-7, so it is similar in cost/efficiency to the Cori cycle |
|
|
Term
| What types of amino acids can be broken down for the synthesis of glucose? |
|
Definition
| Gluconeogenic amino acids |
|
|
Term
| What is the pathway through which amino acids enter gluconeogenesis? |
|
Definition
| They are broken down to any intermediate step of the TCA cycle. Different amino acids are broken down to different steps, and then through the TCA cycle reach oxaloacetate, which can undergo gluconeogenesis |
|
|
Term
| Why can't even number fatty acid rings be broken down to undergo gluconeogenesis? |
|
Definition
| Even numbered rings get broken down to Acetyl-CoA. On its way to Oxaloacetate, the carbons in Acetyl-CoA get burned off as carbon dioxide |
|
|
Term
| How are odd carbon fatty acid rings broken down to enter gluconeogenesis? |
|
Definition
| When they are broken down, there is a 3 carbon Propionate left over. This proprionate goes to Proprionate CoA, to methylmalonyl CoA,to Succinyl CoA, at which point its in the TCA cycle and can head towards oxaloacetate |
|
|
Term
| How is glucose made from glycerol (2 potential pathways) |
|
Definition
Pathway 1:
Glycerol is catabolized down to dihydroxyacetone phosphate, which can join with a glycerol 3-phosphate to make fructose 6 phosphate
Pathway 2:
Glycerol is completely broken down to lactate, which can enter the gluconeogenesis cycle
Note: Which pathway a glycerol takes depends on the degree of catabolism it undergoes. More catabolism leads to lactate. |
|
|
Term
| What compound activates conversion of Pyruvate to Oxaloacetate? |
|
Definition
|
|
Term
| At what level is PEP Carboxylase controlled? What compounds promote its activity and what inhibits it? |
|
Definition
1. It is controlled at the level of gene expression by hormones
2. Insulin inhibits it, whereas glucagon, cortisol, and other corticosteroids promote it |
|
|
Term
| How does F2,6B regulate gluconeogenesis? |
|
Definition
| F2,6B promotes glycolysis, and as such inhibits gluconeogenesis by promoting the activity of PFK-1. Its inhibitory ability is activated by insulin and stopped by glucagon |
|
|
Term
| What effect does diabetes have on gluconeogenesis? |
|
Definition
| It is highly elevated (~3 times normal) |
|
|
Term
| How does gluconeogenesis alter during a fast? |
|
Definition
It increases
(First day of a fast its responsible for 64% body glucose production, by second day essentially all of it) |
|
|
