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Elevated cerebral lactate: Implications in the pathogenesis of hepatic encephalopathy

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Abstract

Hepatic encephalopathy (HE), a complex neuropsychiatric syndrome, is a frequent complication of liver failure/disease. Increased concentrations of lactate are commonly observed in HE patients, in the systemic circulation, but also in the brain. Traditionally, increased cerebral lactate is considered a marker of energy failure/impairment however alterations in lactate homeostasis may also lead to a rise in brain lactate and result in neuronal dysfunction. The latter may involve the development of brain edema. This review will target the significance of increased cerebral lactate in the pathogenesis of HE.

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Notes

  1. Throughout the text, “lactate” will represent L-lactate.

  2. Throughout the text, “LDH” will represent L-LDH.

Abbreviations

HE:

hepatic encephalopathy

MG:

methylglyoxal

LDH:

lactate dehydrogenase

TCA:

tricarboxylic acid cycle

ANLS:

astrocyte-neuron lactate shuttle

BBB:

blood–brain barrier

MCT:

monocarboxylate transporter

ALF:

acute liver failure

CLD:

chronic liver disease

DCA:

dichloroacetate

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Correspondence to Cristina R. Bosoi.

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Bosoi, C.R., Rose, C.F. Elevated cerebral lactate: Implications in the pathogenesis of hepatic encephalopathy. Metab Brain Dis 29, 919–925 (2014). https://doi.org/10.1007/s11011-014-9573-9

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  • DOI: https://doi.org/10.1007/s11011-014-9573-9

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