Research Reports - Human mild traumatic brain injury decreases circulating branched-chain amino acids and their metabolite levels

J Neurotrauma. 2013 Apr 15;30(8):671-9

Jeter CB, Hergenroeder GW, Ward NH 3rd, Moore AN, Dash PK

Abstract The pathophysiology of traumatic brain injury (TBI) is complex and not
well understood. Because pathophysiology has ramifications for injury progression
and outcome, we sought to identify metabolic cascades that are altered after
acute human mild and severe TBI. Because catabolism of branched-chain amino acids
(BCAAs; i.e., valine, isoleucine, and leucine) leads to glucose and energy
metabolism, and neurotransmitter synthesis and availability, we investigated BCAA
metabolites in plasma samples collected within 24 h of injury from mild TBI
(Glasgow Coma Scale [GCS] score >12), severe TBI (GCS ≤8), orthopedic injury, and
healthy volunteers. We report decreased levels of all three BCAAs in patients
with mild TBI relative to healthy volunteers, while these BCAAs levels in
patients with severe TBI were further reduced compared with all groups.
Orthopedic patients exhibited reductions in BCAA comparable to those in patients
with mild TBI. The decrease in patients with mild and severe TBI persisted for
derivatives of BCAA catabolic intermediates. Only plasma levels of
methylglutarylcarnitine, a derivative of a leucine metabolite, were increased in
patients with severe TBI compared with all other groups. Notably, logistic
regression combination of three BCAA metabolites whose levels were changed by
24 h post-injury provided prognostic value (area under the curve=0.92) in
identifying patients with severe TBI in whom elevated intracranial pressure
(≥25 mm Hg) developed. These changes suggest alteration of BCAA metabolism after
TBI may contribute to decreased energy production and neurotransmitter synthesis
and may contribute to TBI pathophysiology. Supplementation of BCAAs and/or their
metabolites may reduce TBI pathology and improve outcome.

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