|Title||A comparison of oxidative lactate metabolism in traumatically injured brain and control brain.|
|Publication Type||Journal Article|
|Year of Publication||2018|
|Authors||Jalloh, I, Helmy, A, Howe, D, Shannon, RJ, Grice, P, Mason, A, Gallagher, CN, Murphy, MP, Pickard, J, Menon, D, Carpenter, TAdrian, Hutchinson, PJohn, Carpenter, K|
|Date Published||2018 Apr 25|
Metabolic abnormalities occur after traumatic brain injury (TBI). Glucose is conventionally regarded as the major energy substrate, although lactate can also be an energy source. We compared 3-13C lactate metabolism in TBI with "normal" control brain and muscle, measuring 13C-glutamine enrichment to assess tricarboxylic acid (TCA) cycle metabolism. Microdialysis catheters in 9 severe TBI patients' brains, 5 non-TBI brain surgical patients, and 5 resting muscle (non-TBI) patients were perfused (24h in brain, 8h in muscle) with 8 mmol/L sodium 3‑13C lactate. Microdialysate analysis employed ISCUS and NMR. In TBI, with 3-13C lactate perfusion, microdialysate glucose concentration increased non-significantly (mean +11.9%, p=0.463), with significant increases (p=0.028) for lactate (+174%), pyruvate (+35.8%), and lactate/pyruvate ratio (+101.8%). Microdialysate 13C-glutamine fractional enrichments (median, IQR) were: for C4 5.1(0-11.1)% in TBI and 5.7(4.6-6.8)% in control brain, for C3 0(0-5.0)% in TBI and 0(0-0) % in control brain, and for C2 2.9(0-5.7)% in TBI and 1.8(0-3.4)% in control brain. 13C-enrichments were not statistically different between TBI and control brain, showing both metabolise 3-13C lactate via TCA cycle, in contrast to muscle. Several TBI patients exhibited 13C-glutamine enrichment above the non-TBI control range, suggesting lactate oxidative metabolism as a TBI "emergency option".
|Alternate Journal||J. Neurotrauma|