Brain energy metabolism and mitochondrial dysfunction in acute and chronic hepatic encephalopathy

Kakulavarapu V. Rama Rao; Michael D. Norenberg

doi:10.1016/j.neuint.2011.09.007

Brain energy metabolism and mitochondrial dysfunction in acute and chronic hepatic encephalopathy

Kakulavarapu V. Rama Rao, Michael D. Norenberg

Research output: Contribution to journal › Review article › peer-review

90 Scopus citations

Abstract

One proposed mechanism for acute and chronic hepatic encephalopathy (HE) is a disturbance in cerebral energy metabolism. It also reviews the current status of this mechanism in both acute and chronic HE, as well as in other hyperammonemic disorders. It also reviews abnormalities in glycolysis, lactate metabolism, citric acid cycle, and oxidative phosphorylation as well as associated energy impairment. Additionally, the role of mitochondrial permeability transition (mPT), a recently established factor in the pathogenesis of HE and hyperammonemia, is emphasized. Energy failure appears to be an important pathogenetic component of both acute and chronic HE and a potential target for therapy.

Original language	English (US)
Pages (from-to)	697-706
Number of pages	10
Journal	Neurochemistry International
Volume	60
Issue number	7
DOIs	https://doi.org/10.1016/j.neuint.2011.09.007
State	Published - Jun 2012
Externally published	Yes

All Science Journal Classification (ASJC) codes

Cellular and Molecular Neuroscience
Cell Biology

Keywords

Ammonia
Astrocytes
Brain edema
Energy metabolism
Hepatic encephalopathy
Mitochondrial permeability transition
Oxidative stress

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10.1016/j.neuint.2011.09.007

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title = "Brain energy metabolism and mitochondrial dysfunction in acute and chronic hepatic encephalopathy",

abstract = "One proposed mechanism for acute and chronic hepatic encephalopathy (HE) is a disturbance in cerebral energy metabolism. It also reviews the current status of this mechanism in both acute and chronic HE, as well as in other hyperammonemic disorders. It also reviews abnormalities in glycolysis, lactate metabolism, citric acid cycle, and oxidative phosphorylation as well as associated energy impairment. Additionally, the role of mitochondrial permeability transition (mPT), a recently established factor in the pathogenesis of HE and hyperammonemia, is emphasized. Energy failure appears to be an important pathogenetic component of both acute and chronic HE and a potential target for therapy.",

keywords = "Ammonia, Astrocytes, Brain edema, Energy metabolism, Hepatic encephalopathy, Mitochondrial permeability transition, Oxidative stress",

author = "{Rama Rao}, {Kakulavarapu V.} and Norenberg, {Michael D.}",

note = "Funding Information: This work was supported by grants from the Department of Veterans Affairs Merit review and the NIH ( DK063311 ). ",

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doi = "10.1016/j.neuint.2011.09.007",

language = "English (US)",

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journal = "Neurochemistry International",

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T1 - Brain energy metabolism and mitochondrial dysfunction in acute and chronic hepatic encephalopathy

AU - Rama Rao, Kakulavarapu V.

AU - Norenberg, Michael D.

N1 - Funding Information: This work was supported by grants from the Department of Veterans Affairs Merit review and the NIH ( DK063311 ).

PY - 2012/6

Y1 - 2012/6

N2 - One proposed mechanism for acute and chronic hepatic encephalopathy (HE) is a disturbance in cerebral energy metabolism. It also reviews the current status of this mechanism in both acute and chronic HE, as well as in other hyperammonemic disorders. It also reviews abnormalities in glycolysis, lactate metabolism, citric acid cycle, and oxidative phosphorylation as well as associated energy impairment. Additionally, the role of mitochondrial permeability transition (mPT), a recently established factor in the pathogenesis of HE and hyperammonemia, is emphasized. Energy failure appears to be an important pathogenetic component of both acute and chronic HE and a potential target for therapy.

AB - One proposed mechanism for acute and chronic hepatic encephalopathy (HE) is a disturbance in cerebral energy metabolism. It also reviews the current status of this mechanism in both acute and chronic HE, as well as in other hyperammonemic disorders. It also reviews abnormalities in glycolysis, lactate metabolism, citric acid cycle, and oxidative phosphorylation as well as associated energy impairment. Additionally, the role of mitochondrial permeability transition (mPT), a recently established factor in the pathogenesis of HE and hyperammonemia, is emphasized. Energy failure appears to be an important pathogenetic component of both acute and chronic HE and a potential target for therapy.

KW - Ammonia

KW - Astrocytes

KW - Brain edema

KW - Energy metabolism

KW - Hepatic encephalopathy

KW - Mitochondrial permeability transition

KW - Oxidative stress

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DO - 10.1016/j.neuint.2011.09.007

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JO - Neurochemistry International

JF - Neurochemistry International

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Brain energy metabolism and mitochondrial dysfunction in acute and chronic hepatic encephalopathy

Abstract

All Science Journal Classification (ASJC) codes

Keywords

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