Changes in metabolomic profile in dogs with hepatic encephalopathy secondary to congenital portosystemic shunt suggests mitochondrial homeostasis disturbances.

Dogs with hepatic encephalopathy show metabolomic evidence of mitochondrial dysfunction, suggesting mitochondrial support as a potential novel therapy.

This prospective observational study investigated serum metabolomic changes in dogs with congenital portosystemic shunt (CPSS), comparing those with hepatic encephalopathy (HE) signs to those without, and evaluating metabolite normalization following medical treatment. Ten client-owned dogs with CPSS were enrolled between March 2021 and October 2022. Serum samples were analyzed using ultra-performance liquid chromatography-mass spectrometry (UPLC-MS). Dogs exhibiting HE signs (n=6) demonstrated significantly lower serum concentrations of taurine (FC 0.44), creatine (FC 0.32), and guanine (FC 0.45), alongside significantly elevated 3-hydroxybenzaldehyde (FC 2.51) compared to non-HE dogs (n=4). A marked, though statistically non-significant, reduction in stearate was also noted (FC 0.12). These metabolite alterations collectively suggest disruption of mitochondrial homeostasis, as taurine, creatine, and stearate all play roles in mitochondrial function and energy metabolism. Importantly, following at least four weeks of medical management that clinically improved neurological signs, these metabolite concentrations—particularly taurine—normalized toward levels observed in non-HE dogs. The findings highlight a distinct metabolomic signature in dogs with HE secondary to CPSS and propose mitochondrial dysfunction as a potential underlying mechanism. The authors suggest that targeting mitochondrial support, potentially through taurine supplementation or related strategies, could represent a novel therapeutic avenue. Limitations include small sample size and the observational design, warranting larger controlled studies to validate these findings and explore targeted mitochondrial therapies.

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