Modulation of brain energy metabolism in hepatic encephalopathy: impact of glucose metabolic dysfunction.
Level 5 - mechanism / opinion, no new human data
Narrative review of mechanism-based biology without systematic review methodology or primary data.
PubMed 39120853 · doi:10.1007/s11011-024-01407-7
What was done
This narrative review synthesized literature on cerebral energy metabolism in hepatic encephalopathy, examining how hyperammonemia alters glucose metabolic pathways—including glycolysis, glycogen metabolism, lactate metabolism, the pentose phosphate pathway, and the Krebs cycle—and disrupts metabolic cooperation between brain cell types.
What was found
The abstract reports no quantitative metrics or empirical data. It summarizes mechanistic pathways through which ammonia-induced disruption of glucose metabolism compromises brain bioenergetics, leading to neuronal death and clinical manifestations ranging from subclinical abnormalities to coma.
Why it matters
It outlines how bioenergetic failure contributes to hepatic encephalopathy pathogenesis, identifying brain glucose metabolism regulation as a potential target for novel diagnostic and therapeutic development.
Limits
The paper is a non-systematic narrative review with no formal search strategy, study selection criteria, or quantitative synthesis. No primary human or animal data are presented in the abstract.
Cited by
- supports Glucose is the primary fuel source for human cells, especially brain cells.