Glycogenolysis, Lipolysis and Gluconeogenesis Flashcards
lecture 5
Euglycemia
Normal
* ~ 5 mM (>4mM)
Can the brain use FAs?
No, cannot cross blood-brain barrier
Glucose usage of brain
~ 120g/day
* GLUT-1
Pyruvate > acetyl CoA is irreversible
TRUE
first few hrs of starvation
Uptake of glucose in tissue
* blood glucose ↓
* liver release glucose - maintain euglycemia
signal for glycogenolysis
Binding of glucagon to receptors on the liver cell membrane
* GLUT-2 very active
Glycogenolysis
Phosphorylase breaks down glycogen
* Phosphorolysis - cleavage using P
* Produces G 1-P
* Rapidly converted into G 6-P
Amplification in glycogenolysis
Amp. thru 2nd messenger and cascade
* each step catalysed by an enzyme
* more control
* massive response from small signal
Debranching enzyme
- At the branch points, simple hydrolysis used
- About 10% of glucose residues are relased as glucose (NOT glucose-1-P)
Muscle does NOT breakdown glycogen in starvation because:
- No glucagon receptors
- No G6Pase, therefore cannot convert G6P > Glucose or release in blood
- However some residues in glycogen released as “neat” glucose - debranching enzyme uses water to hydrolyse the glycosidic linkages, not phosphate (10% released this way)
Glycogen depletion
Glycogen store in liver - 100g (brain will use it up in <24hr
* Need to persuade other tissue to use fat rather than glucose well before liver depletion
* Active WAT - fatty acids
WAT lipolysis
Glucagon > ↑[cAMP] > ↑ activity of PKA
* PKA phosphorylates hormone sensituve lipase (activates) + perilipin
* Allow HSL to interact w/ fat
* FA released in blood
FAs are oxidised to…
Proved AcCoA for Krebs
* avoid oxidation of glucose
In starvation we want PDH to be…
OFF
* PDH kinase activity»_space; PDH phosphatase activity
* PDH kinase stimulated by AcCoA
* PDH inactive when phosphorylated
* Prevents wasteful oxidation of pyruvate (only to lactate)
Fate of lactate when pyruvate cannot be oxidised
Taken up in liver
* gluconeogenesis
* conservation
* Cori-cycle
