Gene expression of glucose transporters and glycolytic enzymes in the CNS of rats behaviorally dependent on ethanol

Eravci, Murat; Kley, Stefan; Pinna, Graziano; Prengel, Hans; Brödel, Oliver; Hiedra, Luis; Meinhold, H.; Baumgartner, Andreas

doi:10.1016/s0169-328x(98)00347-7

Cited by 16 publications

(10 citation statements)

References 52 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Each of these proteins plays an important role in glycolysis, a 10-step energy metabolism pathway that converts glucose into high energy molecules (ATP and NADH) and pyruvate (to be used in the Krebs cycle). A previous study also using Wistar rats found chronic alcohol consumption reduced the gene expression of glycolytic enzymes and glucose transporters in the hippocampus (Eravci et al, 1999). Similarly, past proteomic studies have shown that alcohol alters glycolytic enzymes in the mouse brain (Park et al, 2004), in the amygdala (Bell et al, 2006a) and liver of alcohol-preferring rats (Klouckova et al, 2006;Nomura et al, 2007), and in postmortem analysis of the human alcoholic hippocampus (Matsuda-Matsumoto et al, 2007), corpus collosum , cerebellum (Alexander-Kaufman et al, 2007b), frontal gray matter (Alexander-Kaufman et al, 2007a), and frontal white matter (Alexander-Kaufman et al, 2006).…”

Section: Reduced Glycolysismentioning

confidence: 83%

“…For instance, self-administration of alcohol causes more protein changes than forced alcohol intake (Eravci et al, 1999), just as a schedule of intermittent rather than continuous alcohol access produces greater neural changes (Bell et al, 2006a;Sari et al, 2006). Given the propensity for human adolescents to binge drink (White and Hayman, 2004), the protocol employed in the present study, where rats were given voluntary access to beer for 8 hours each day rather than continuous or forced access, was intended to reflect the typical stop-start pattern of alcohol intake observed in teenage drinkers.…”

Section: Alcohol Consumptionmentioning

confidence: 99%

See 1 more Smart Citation

Proteomic Analysis Demonstrates Adolescent Vulnerability to Lasting Hippocampal Changes Following Chronic Alcohol Consumption

Hargreaves

Quinn

Kashem

et al. 2008

Alcoholism Clin & Exp Res

View full text Add to dashboard Cite

Background: Excessive teenage alcohol consumption is of great concern because alcohol may adversely alter the developmental trajectory of the brain. The aim of the present study was to assess whether chronic intermittent alcohol intake during the adolescent period alters hippocampal protein expression to a greater extent than during adulthood.Methods: Adolescent [postnatal day (PND) 27] and adult (PND 55) male Wistar rats were given 8 hours daily access to beer (4.44% ethanol v ⁄ v) in addition to ad libitum food and water for 4 weeks. From a large subject pool, subgroups of adolescent and adult rats were selected that displayed equivalent alcohol intake (average of 6.1 g ⁄ kg ⁄ day ethanol). The 4 weeks of alcohol access were followed by a 2-week alcohol-free washout period after which the hippocampus was analyzed using 2-DE proteomics.Results: Beer consumption by the adult group resulted in modest hippocampal changes relative to alcohol naı¨ve adult controls. The only changes observed were an up-regulation of citrate synthase (a precursor to the Krebs cycle) and fatty acid binding protein (which facilitates fatty acid metabolism). In contrast, adolescent rats consuming alcohol showed more widespread hippocampal changes relative to adolescent controls. These included an increase in cytoskeletal protein T-complex protein 1 subunit epsilon (TCP-1) and a decrease in the expression of 10 other proteins, including glyceraldehyde-3-phosphate dehydrogenase (GAPDH), triose phosphate isomerise, alpha-enolase, and phosphoglycerate kinase 1 (all involved in glycolysis); glutamate dehydrogenase 1 (an important regulator of glutamate); methylmalonate-semialdehyde dehydrogenase (involved in aldehyde detoxification); ubiquitin carboxyl-terminal hydrolase isozyme L1 (a regulator of protein degradation); and synapsin 2 (involved in synaptogenesis and neurotransmitter release).Conclusions: These results suggest the adolescent hippocampus is more vulnerable to lasting proteomic changes following repeated alcohol exposure. The proteins most affected include those related to glycolysis, glutamate metabolism, neurodegeneration, synaptic function, and cytoskeletal structure.

show abstract

Section: Reduced Glycolysismentioning

confidence: 83%

Section: Alcohol Consumptionmentioning

confidence: 99%

Proteomic Analysis Demonstrates Adolescent Vulnerability to Lasting Hippocampal Changes Following Chronic Alcohol Consumption

Hargreaves

Quinn

Kashem

et al. 2008

Alcoholism Clin & Exp Res

View full text Add to dashboard Cite

show abstract

“…It should be noted that in the present study we tested the concentration, but not the activity, of key glycolytic enzymes in order to evaluate the long-term changes in protein levels resulting from abnormal gene expression. Indeed, changes in the expression of genes encoding glycolytic enzymes and glucose transporters were found after imipramine administration for 8 weeks and in animals dependent on ethanol (Eravci et al, 1999;Wong et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

Brain glucose metabolism in an animal model of depression

et al. 2015

View full text Add to dashboard Cite

“…Taken together, these data highlight the heterogeneity of alcoholrelated encephalopathies [66] and indicate a possible link between the high brain scyllo-Ins level and brain defective glucose metabolism in chronic alcoholics. In animal models of alcoholism, an inhibition of the glycolytic flux due to a reduction of gene expression of neuronal glucose transporters and phosphofructokinase (the pacemaker of glycolysis) has been reported [67]. In mice transgenic for exon 1 of mutant huntingtin [68] showing high concentrations of brain glucose caused by a defective brain glycolysis, brain MRS has evidenced a collapse of NAA, an increase in glutamine and Cho and a large augmentation of scyllo-Ins.…”

Section: Discussionmentioning

confidence: 99%

High cerebral scyllo-inositol: a new marker of brain metabolism disturbances induced by chronic alcoholism

Viola

Nicoli

Denis

et al. 2004

MAGMA

View full text Add to dashboard Cite

Cerebral metabolic changes that concur to motor and/or cognitive disorders in actively drinking alcoholics are not well established. We tested the hypothesis that chronic alcoholics exhibit profound alterations in the cerebral metabolism of scyllo-inositol. Brain metabolism was explored in nine actively drinking and 11 recently detoxified chronic alcoholics by in vivo brain 1 H-MRS and in vitro 1 H-MRS of blood serum and cerebrospinal fluid. The cohort was composed of individuals with acute, subacute or chronic encephalopathy or without any clinical encephalopathy. Chronic alcoholism is associated with a hitherto unrecognized accumulation of brain scyllo-inositol. Our results suggest that scyllo-inositol is produced within the central nervous system and shows a diffuse but heterogenous distribution in brain where it can persist several weeks after detoxification. Its highest levels were observed in subjects with a clinically symptomatic alcohol-related encephalopathy. When detected, brain scyllo-inositol takes part in a metabolic encephalopathy since it is associated with reduced N-acetylaspartate and increased creatine. High levels of cerebral scyllo-inositol are correlated with altered glial and neuronal metabolism. Our findings suggest that the accumulation of scyllo-inositol may precede and take part in the development of symptomatic alcoholic metabolic encephalopathy.

show abstract

Gene expression of glucose transporters and glycolytic enzymes in the CNS of rats behaviorally dependent on ethanol

Cited by 16 publications

References 52 publications

Proteomic Analysis Demonstrates Adolescent Vulnerability to Lasting Hippocampal Changes Following Chronic Alcohol Consumption

Proteomic Analysis Demonstrates Adolescent Vulnerability to Lasting Hippocampal Changes Following Chronic Alcohol Consumption

Brain glucose metabolism in an animal model of depression

High cerebral scyllo-inositol: a new marker of brain metabolism disturbances induced by chronic alcoholism

Contact Info

Product

Resources

About