ArticleFrontiers in neuroscience2014
Oxidative metabolism of astrocytes is not reduced in hepatic encephalopathy: a PET study with [(11)C]acetate in humans.
Article in Frontiers in neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.
- Correlation of ammonia and blood laboratory parameters with hepatic encephalopathy: A systematic review and meta-analysis.PloS one · 2024Pooled it
- Fueling Brain Inhibition: Integrating GABAergic Neurotransmission and Energy Metabolism.Neurochemical research · 2025Review
- Hepatic encephalopathy as a result of ammonia-induced increase in GABAergic tone with secondary reduced brain energy metabolism.Metabolic brain disease · 2024Review
- Ammonia-induced stress response in liver disease progression and hepatic encephalopathy.Nature reviews. Gastroenterology & hepatology · 2024Review
- The role of brain inflammation and abnormal brain oxygen homeostasis in the development of hepatic encephalopathy.Metabolic brain disease · 2023Review
- Does ammonia really disrupt brain oxygen homeostasis?JHEP reports : innovation in hepatology · 2023Article
- Abnormal brain oxygen homeostasis in an animal model of liver disease.JHEP reports : innovation in hepatology · 2022Article
- Glutamate Dehydrogenase Is Important for Ammonia Fixation and Amino Acid Homeostasis in Brain During Hyperammonemia.Frontiers in neuroscience · 2021Article
- Impaired brain function improved by L-carnitine in patients with cirrhosis: evaluation using near-infrared spectroscopy.Scientific reports · 2020Article
- The roles ofEuropean journal of nuclear medicine and molecular imaging · 2018Article
- Accumulation of lactate in the rat brain during hyperammonaemia is not associated with impaired mitochondrial respiratory capacity.Metabolic brain disease · 2017Article
- Neurotoxicity of Ammonia.Neurochemical research · 2017Review
- Multifactorial Effects on Different Types of Brain Cells Contribute to Ammonia Toxicity.Neurochemical research · 2017Review
- Kinetic study of benzyl [1-14C]acetate as a potential probe for astrocytic energy metabolism in the rat brain: Comparison with benzyl [2-14C]acetate.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2016Article
- Ammonia Affects Astroglial Proliferation in Culture.PloS one · 2015Article
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In patients with impaired liver function and hepatic encephalopathy (HE), consistent elevations of blood ammonia concentration suggest a crucial role in the pathogenesis of HE. Ammonia and acetate are metabolized in brain both primarily in astrocytes. Here, we used dynamic [(11)C]acetate PET of the brain to measure the contribution of astrocytes to the previously observed reduction of brain oxidative metabolism in patients with liver cirrhosis and HE, compared to patients with cirrhosis without HE, and to healthy subjects. We used a new kinetic model to estimate uptake from blood to astrocytes and astrocyte metabolism of [(11)C]acetate. No significant differences of the rate constant of oxidation of [(11)C]acetate (k 3) were found among the three groups of subjects. The net metabolic clearance of [(11)C]acetate from blood was lower in the group of patients with cirrhosis and HE than in the group of healthy subjects (P < 0.05), which we interpret to be an effect of reduced cerebral blood flow rather than a reflection of low [(11)C]acetate metabolism. We conclude that the characteristic decline of whole-brain oxidative metabolism in patients with cirrhosis with HE is not due to malfunction of oxidative metabolism in astrocytes. Thus, the observed decline of brain oxidative metabolism implicates changes of neurons and their energy turnover in patients with HE.
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