ArticleMolecular and cellular biochemistry2013
Moderate grade hyperammonemia activates lactate dehydrogenase-4 and 6-phosphofructo-2-kinase to support increased lactate turnover in the brain slices.
Article in Molecular and cellular biochemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 15 citations in OpenAlex.
- Association of serum lactate dehydrogenase levels with non-alcoholic fatty liver disease and advanced hepatic fibrosis in the United States: a cross-sectional study using NHANES data from 2007 to 2018.BMC gastroenterology · 2025Article
- Modulation of brain energy metabolism in hepatic encephalopathy: impact of glucose metabolic dysfunction.Metabolic brain disease · 2024Review
- Hepatic Encephalopathy and Melatonin.Antioxidants (Basel, Switzerland) · 2022Review
- Serum lactate dehydrogenase activities as systems biomarkers for 48 types of human diseases.Scientific reports · 2021Article
- Multifactorial Effects on Different Types of Brain Cells Contribute to Ammonia Toxicity.Neurochemical research · 2017Review
- Acute Hyperammonemia Induces NMDA-Mediated Hypophosphorylation of Intermediate Filaments Through PP1 and PP2B in Cerebral Cortex of Young Rats.Neurotoxicity research · 2016Article
- Pannexin1 as a novel cerebral target in pathogenesis of hepatic encephalopathy.Metabolic brain disease · 2014Article
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2 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Rapid metabolism of lactate is an important aspect of bioenergetic adaptation in the brain during non-physiological conditions. The low grade hyperammonemia (HA) is a common condition in the patients with chronic hepatic encephalopathy (HE); however, biochemistry of lactate turnover during low grade HA remains poorly defined. The present article describes profile of lactate dehydrogenase (LDH) isozymes vis-a-vis lactate level in the brain slices exposed with 0.1-0.5 mM ammonia, found to exist in the brain during chronic HE. A significant increment in LDH activity coincided with a similar increase in lactate level in the brain slices exposed with 0.5 mM ammonia. This was consistent with a selective increment of LDH-4 that synthesizes lactate from pyruvate with a concomitant decline in LDH-1 which catalyzes conversion of lactate to pyruvate; resulting into ~3-fold increase in LDH-4/LDH-1 ratio in those brain slices. The PFK2 domain of PFK2/FBPase2 (6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase) regulates glycolysis to maintain the pyruvate pool for lactate synthesis. The PFK2 expression was also observed to be increased ~2-fold (P < 0.001) in 0.5 mM ammonia treated brain slices. These findings provide enzymatic regulation of increased lactate turnover in the brain exposed with moderate HA.
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