Hepatic immunometabolic response to traumatic brain injury measured by hyperpolarized [1-13C]pyruvate

Motivation: TBI disrupts brain glucose metabolism, leading to systemic metabolic adaptations. Goal(s): To assess immunometabolic adaptations in the liver induced by TBI under different nutritional states. Approach: The hepatic metabolism of two groups of rats (TBI and control) was investigated using hyperpolarized [1-13C]pyruvate under fed and fasted conditions. The levels of 13C-labeled lactate, alanine, aspartate, and bicarbonate were compared between the groups. Results: Bicarbonate and aspartate production increased in the TBI group under fasting, suggesting that gluconeogenic pathway was activated post-TBI. Impact: This study demonstrates that acute phase response of the liver to TBI can be monitored by hyperpolarized pyruvate in vivo. The proposed method can be further utilized for longitudinal immunometabolic evaluation of the liver during pathogenesis and therapeutic interventions.