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Int J Physiol Pathophysiol Pharmacol 2011;3(1):48-56.
Original Article
Ethanol impairs glucose uptake by human astrocytes and neurons: protective
effects of acetyl-L-carnitine
P. M. Abdul Muneer, Saleena Alikunju, Adam M. Szlachetka, Aaron Mercer, James Haorah
Department of Pharmacology and Experimental Neuroscience, Department of Ophthalmology and Visual Science, University of
Nebraska Medical Center, Omaha, NE 68198, USA.
Received December 23, 2010; accepted December 26, 2010; Epub December 27, 2010; Published January 1, 2011
Abstract: Alcohol consumption causes neurocognitive deficits, neuronal injury, and neurodegeneration. At the cellular level, alcohol
abuse causes oxidative damage to mitochondria and cellular proteins and interlink with the progression of neuroinflammation and
neurological disorders. We previously reported that alcohol inhibits glucose transport across the blood-brain barrier (BBB), leading to
BBB dysfunction and neurodegeneration. In this study, we hypothesized that ethanol (EtOH)-mediated disruption in glucose uptake
would deprive energy for human astrocytes and neurons inducing neurotoxicity and neuronal degeneration. EtOH may also have a
direct effect on glucose uptake in neurons and astrocytes, which has not been previously described. Our results indicate that ethanol
exposure decreases the uptake of D-(2-3H)-glucose by human astrocytes and neurons. Inhibition of glucose uptake correlates with a
reduction in glucose transporter protein expression (GLUT1 in astrocytes and GLUT3 in neurons). Acetyl-L-carnitine (ALC), a
neuroprotective agent, suppresses the effects of alcohol on glucose uptake and GLUT levels, thus reducing neurotoxicity and neuronal
degeneration. These findings suggest that deprivation of glucose in brain cells contributes to neurotoxicity in alcohol abusers, and
highlights ALC as a potential therapeutic agent to prevent the deleterious health conditions caused by alcohol abuse. (IJPPP1012003).
Key words: Human astrocytes, glucose transporter protein, acetyl-L-carnitine, neurodegeneration
Full Text PDF
Address all correspondence to:
Dr. James Haorah
Laboratory of Neurovascular Oxidative Injury,
Department of Pharmacology and Experimental Neuroscience,
University of Nebraska Medical Center, Omaha, NE 68198.
Phone: 001-402-559-5406
Fax: 001-402-559-8922,
Email: jhaorah@unmc.edu
Original Article
Ethanol impairs glucose uptake by human astrocytes and neurons: protective
effects of acetyl-L-carnitine
P. M. Abdul Muneer, Saleena Alikunju, Adam M. Szlachetka, Aaron Mercer, James Haorah
Department of Pharmacology and Experimental Neuroscience, Department of Ophthalmology and Visual Science, University of
Nebraska Medical Center, Omaha, NE 68198, USA.
Received December 23, 2010; accepted December 26, 2010; Epub December 27, 2010; Published January 1, 2011
Abstract: Alcohol consumption causes neurocognitive deficits, neuronal injury, and neurodegeneration. At the cellular level, alcohol
abuse causes oxidative damage to mitochondria and cellular proteins and interlink with the progression of neuroinflammation and
neurological disorders. We previously reported that alcohol inhibits glucose transport across the blood-brain barrier (BBB), leading to
BBB dysfunction and neurodegeneration. In this study, we hypothesized that ethanol (EtOH)-mediated disruption in glucose uptake
would deprive energy for human astrocytes and neurons inducing neurotoxicity and neuronal degeneration. EtOH may also have a
direct effect on glucose uptake in neurons and astrocytes, which has not been previously described. Our results indicate that ethanol
exposure decreases the uptake of D-(2-3H)-glucose by human astrocytes and neurons. Inhibition of glucose uptake correlates with a
reduction in glucose transporter protein expression (GLUT1 in astrocytes and GLUT3 in neurons). Acetyl-L-carnitine (ALC), a
neuroprotective agent, suppresses the effects of alcohol on glucose uptake and GLUT levels, thus reducing neurotoxicity and neuronal
degeneration. These findings suggest that deprivation of glucose in brain cells contributes to neurotoxicity in alcohol abusers, and
highlights ALC as a potential therapeutic agent to prevent the deleterious health conditions caused by alcohol abuse. (IJPPP1012003).
Key words: Human astrocytes, glucose transporter protein, acetyl-L-carnitine, neurodegeneration
Full Text PDF
Address all correspondence to:
Dr. James Haorah
Laboratory of Neurovascular Oxidative Injury,
Department of Pharmacology and Experimental Neuroscience,
University of Nebraska Medical Center, Omaha, NE 68198.
Phone: 001-402-559-5406
Fax: 001-402-559-8922,
Email: jhaorah@unmc.edu
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