Covers energy metabolism in leukocytes, which unlike red cells can use the TCA cycle, oxidative phosphorylation and fatty acid oxidation, then shifts to anaerobic glycolysis during inflammation (the Warburg effect). It then explains the NADPH-driven respiratory burst, the role of NADPH oxidase and myeloperoxidase, and the infections linked to CGD. The note turns to platelets, which keep mitochondria despite lacking a nucleus, and to thromboxane A2 production via COX-1, with aspirin's lasting inhibition. It ends with brief clinical links to warfarin, aspirin and CGD.
Topic 66 of 76 in the MU Pleven syllabus for Biochemistry (Medicine, Year 2). The free AceMed note covers it in 4 sections, about 330 words (2 min of reading), with 13 flashcards.
In this note
Metabolism in Leukocytes (WBC) and Platelets.
Metabolism in Leukocytes (WBCs)
Metabolism in Platelets
Clinical Links
Metabolism in Leukocytes (WBCs)
Leukocytes are nucleated cells and contain mitochondria, so unlike RBCs, they can use: – Aerobic glycolysis – Krebs cycle (TCA cycle) – Oxidative phosphorylation – Fatty acid oxidation (especially in resting / non-activated states)
During inflammation or infection, activated leukocytes switch to anaerobic glycolysis, even when oxygen is available. This is called the Warburg effect and supports rapid energy production during immune response.
Glucose uptake increases in activated leukocytes and is insulin-independent, mediated by GLUT1 and GLUT3.
During phagocytosis, neutrophils produce NADPH through the Pentose Phosphate Pathway. NADPH is needed for the respiratory burst.
Respiratory Burst: – Enzyme: NADPH oxidase – Generates superoxide (O₂⁻), which is converted to hydrogen peroxide and hypochlorous acid (HOCl) by myeloperoxidase (MPO). – These reactive oxygen species kill pathogens.
Defect in NADPH oxidase → Chronic Granulomatous Disease (CGD)
Leads to recurrent bacterial & fungal infections.
Defect in MPO → Reduced microbial killing, but typically milder than CGD.
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