Kupffer cells modulate hepatic fatty acid oxidation during infection with PR8 influenza.

ABSTRACT: In response to infection, patients with inborn errors of metabolism may develop a functional deterioration termed metabolic decompensation. The biochemical hallmarks of this disruption of metabolic homeostasis are disease specific and may include acidosis, hyperammonemia or hypoglycemia. In a model system previously published by our group, we noted that during influenza infection, mice displayed a depression in hepatic mitochondrial enzymes involved in nitrogen metabolism. Based on these findings, we hypothesized that this normal adaptation may extend to other metabolic pathways, and as such, may impact various inborn errors of metabolism. Since the liver is a critical organ in inborn errors of metabolism, we carried out untargeted metabolomic profiling of livers using mass spectrometry in

SUBMITTER: Tarasenko TN 

PROVIDER: S-EPMC6662236 | biostudies-literature | 2015 Nov

REPOSITORIES: biostudies-literature