Lecture 8 Flashcards
(6 cards)
Use of G6Pase in diagnostics
G6Pase exists only in liver. In PET scans, cells take up radioactive 2-deoxyglucose (FdG), which is phosphorylated to 6-phospho-FdG. Because it lacks an OH at the 2’ position, it can’t continue through glycolysis and accumulates. Cancer cells, which consume lots of glucose, trap more 6-phospho-FdG, making them visible on scans. The tracer is cleared via urine, so the bladder and brain often appear black.
Role of amino acid skeletons in oxaloacetate supply
If oxaloacetate were used only for gluconeogenesis, the Krebs cycle would run out of intermediates. To maintain it, some amino acids are broken down into carbon skeletons that replenish oxaloacetate. This allows acetyl-CoA to continue entering the cycle, supporting energy production even during active glucose synthesis.
Role of F2,6BP in metabolic regulation
F2,6BP is a powerful regulator that does not enter metabolism directly. When present, it activates glycolysis and inhibits gluconeogenesis. When absent, gluconeogenesis proceeds. Its levels can shift rapidly to change metabolic direction
F2,6BP’s effects on key enzymes
F2,6BP stimulates PFK-1 to promote glycolysis and inhibits fructose 1,6-bisphosphatase to block gluconeogenesis. When F2,6BP levels increase, glycolysis is favoured; when it drops, gluconeogenesis is activated.
Hormonal control of F2,6BP
A single bifunctional enzyme (PFK-2/FBPase-2) makes or breaks F2,6BP. Its activity depends on hormonal signalling:
Insulin activates phospho-protein phosphatase (PPP), stimulating PFK-2 → F2,6BP made → glycolysis on.
Glucagon activates cAMP-dependent protein kinase (PKA), stimulating FBPase-2 → F2,6BP broken down → gluconeogenesis on.
Both PKA and PPP are tightly regulated.
Gluconeogenesis during starvation
During starvation, glucagon rises, increasing cAMP. This decreases F2,6BP levels. As a result, PFK-1 is no longer stimulated, so glycolysis slows. At the same time, FBPase is no longer inhibited, allowing gluconeogenesis to proceed.
