Hepatic encephalopathy (HE) is a severe complication of chronic liver disease which drastically affects patient lives. Its underlying mechanisms are still unknown and energy metabolism studies are of key interest. Here, we combined 18F-FDG PET and 1H-MRS and found a 2-fold decrease in brain glucose uptake in a rat model of HE compared to SHAM rats, associated with a previously reported increase in brain glutamine and decrease in osmolytes. Although the difference in glucose uptake measured by PET results from a combination of brain and systemic effects, this finding provides a new perspective on HE pathophysiology.
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