Role of ammonia and glutamine in the pathogenesis and progression of metabolic dysfunction-associated steatotic liver disease: A systematic review.
Level 5 - mechanism / opinion, no new human data
Systematic review synthesizing predominantly mechanistic and preclinical evidence with no human clinical trials.
PubMed 38763916 · doi:10.1111/jgh.16603
What was done
A systematic review (PROSPERO CRD42023495619) searched five major databases through December 21, 2023, for studies examining ammonia or glutamine in relation to metabolic dysfunction-associated steatotic liver disease (MASLD). Study quality was appraised using CASP checklists following PRISMA guidelines.
What was found
The review included 13 studies. The abstract provides no numerical data, pooled effect sizes, or statistical metrics. Findings qualitatively showed variable expression of glutamine synthetase and glutaminase enzymes and implicated urea cycle dysfunction in ammonia accumulation, with an acknowledged lack of human clinical trials.
Why it matters
This review synthesizes mechanistic evidence implicating ammonia and glutamine dysregulation in MASLD progression, highlighting potential metabolic pathways for future drug development.
Limits
The abstract reports no quantitative results. The underlying evidence base consists primarily of preclinical and mechanistic studies, with a complete absence of human clinical trials. Sample sizes and study designs across the 13 included studies were heterogeneous.
Cited by
- supports Supplemental glutamine can be converted in the body into both glutamate and ammonia.