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In the HMP shunt, glucose-6-phosphate, which normally proceeds through glycolysis, can instead be shunted through this side-pathway to produce numerous intermediates and NADPH.
The USMLE gives a fuck about NADPH because this molecule plays an important role in the respiratory burst and the regeneration of reduced glutathione. Reduced glutathione is protective against oxidizing agents and helps keep RBC membranes stable.
The rate-limiting enzyme that allows for this shunting to occur is glucose-6-phosphate dehydrogenase (G6PD).
Therefore, G6PD deficiency → ↓NADPH → hemolysis in the event of stressors such as drugs, fava beans, DKA, infection, trauma.
Finally, transketolase is used to recycle excess HMP intermediates back to fructose-6-phosphate in glycolysis. This enzyme is thiamine-dependent.
| If someone is administered thiamine in the setting of suspected deficiency and they tell you transketolase activity increases <5%, it means the patient did not have thiamine deficiency. If enzyme activity increases >15%, that means there was severe deficiency. |
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