Random high yield things from Bessesen lectures Flashcards
In what way is gluconeogenesis different from glycolysis?
- It runs in reverse
- Goes from pyruvate –> oxaloacetate –> PEP instead of straight backwards
Kids who can’t burn fat via TCA cycle present as what?
Hyperglycemia
What tissue is most important source of glucose in blood?
Liver & Kidney because have G6P-ase (enzyme). Liver > Kidney
What pathway level is responsible for a diabetic increased glucose level?
Gluconeogenesis
What is the source of the carbons that make the glucose that is in a fasting diabetic’s blood?
Lactate from RBCs
If a baby can’t sleep through the night, what is happening?
He is fasting and gets a neurologic problem. Depends upon his liver to produce glucose for his brain.
Tissues and glycogen
Muscle - its own use
Liver - whole body
Where does the glycogen pathway start and end?
Starts at glycogen
Ends at glucose-6-P (which goes on to glucose)
Explain coordinate regulation of glycogen
You are either going to make glycogen or break it down, you won’t do both together
UDP is a ___ form of glucose
high energy
What is function of branched structure of glycogen
- Rapid mobilization to glucose
2. Rapid storage as glycogen
What serves as a protein anchor to start glycogen chain?
Glycogenin
Which enzymes are critical for glycogen formation?
Glycogen synthase; only gives linear 1-4 structure. You need a branching enzyme (4:6 transferase) that counts 5 glucoses in to make a 1-6 bond for the branch.
Contrast the functions of glycogen in the liver vs. muscle
- Liver -> has glucose-6-phosphatase and can therefore turn it into glucose for the blood. 400g, doesn’t last you very long
- Muscle - does not have the G6P enzyme, so it ends up using glycogen (via G6P input into glycolysis) for energy
Key steps of glycogen (forward and backward pathway)
- Forward to glycogen: Glycogen synthase from UDP-glucose –> Glycogen
Branching enzyme as well. - Backward to G6P: Glycogenphosphorylase for Glycogen –> Glucose 1-P
Debranching enzyme as well.
In the liver, what things inhibit glycogen breakdown?
- Glucose
- ATP
- G6P
In the muscle, what things inhibit & stimulate glycogen breakdown?
- G6P - inhibit
- ATP - inhibit
These are indicators of exercise, which should stimulate breakdown
- Ca++ - stimulate
- AMP - stimulate
Covalent modifiers of glycogen phosphorylase
- Glucagon phosphorylates glycogen phosphorylase via phosphorylation of glycogen phosphorylase kinase –> glycogen breakdown
- Insulin dephosphorylates glycogen phosphorylase kinase and glycogen phosphorylase (by glycogen phosphorylase kinase)
When is glycogen phosphorylase kinase active? What is its role?
Active when it is phosphorylated
Role: put a phosphate group on glycogen phosphorylase to make it active
Catabolic vs. Anabolic
Catabolic: associated with energy
Anabolic: associated with structure & function
2 functions of HMP Shunt
- Make NADPH (for synthesis of lipids)
2. 5-C skeleton (ribose sugars) for nucleotide synthesis
Young patient comes in, treated for a UTI with a sulfa drug. They were jaundiced at birth and now have increased retic count, indirect bili, and free Hgb. What is the most likely cause of her problem? Why?
She is G6PD deficient
Gets a hemolytic anemia because it is necessary for the regeneration of NADP+ from glutathione reductase. Cannot relive the oxidant stress of drugs without G6PD.
How can you distinguish between insulin you give someone and the insulin they make?
Measure C-peptide as this is the molecule of endogenous insulin production
Actions of insulin
- Increase glucose uptake into muscle
- Increase glycogen synthesis
- Mitogen
- Na+ and H20 retention
- Inhibits lipolysis
- Inhibits ketogenesis
- Changes blood flow
GLP-1
- Product of proglucagon gene from intestinal L-cells
- Release is rapid in response to meals
- Potent insulinotropic hormone (requires glucose to stimulate insulin secretion, this just potentiates it)
- Impaired glucose tolerance and T2D manifest with lower plasma GLP-1 than controls
3 hormones playing a role in T2D
- Relative insulin deficiency
- Relative glucagon excess
- Relative GLP-1 deficiency