Database : MEDLINE
Search on : Alcohol-Induced and Disorders [Words]
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[PMID]: 29266790
[Au] Autor:Guo X; Chen M; Zeng H; Liu P; Zhu X; Zhou F; Liu J; Zhang J; Dong Z; Tang Y; Gao C; Yao P
[Ad] Address:Department of Nutrition and Food Hygiene, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
[Ti] Title:Quercetin Attenuates Ethanol-Induced Iron Uptake and Myocardial Injury by Regulating the Angiotensin II-L-Type Calcium Channel.
[So] Source:Mol Nutr Food Res;62(5), 2018 Mar.
[Is] ISSN:1613-4133
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:SCOPE: Increased iron deposition in the myocardium in alcoholics may lead to increased risk of cardiac dysfunction. Quercetin has been demonstrated to quench production of intracellular free iron-induced -OH, but the effect of quercetin in ethanol-induced cardiac damage remains unclear. This study aims to explore whether quercetin attenuates ethanol-induced iron uptake and myocardial injury by regulating angiotensin II-L-type voltage-dependent Ca2+ channel (Ang II-LTCC). METHODS AND RESULTS: Adult male C57BL/6J mice are isocalorically pair-fed either a regular or ethanol-containing Lieber De Carli liquid diets supplemented with either quercetin (100 mg kg  bw) or desferrioxamine mesylate (DFO, 100 mg kg bw) for 15 weeks. Quercetin alleviated ethanol-induced histopathological changes, creatine kinase isoenzyme release, Ang II secretion, ROS generation, total cardiac iron, and labile iron level. Ethanol exposure or quercetin intervention fails to regulate traditional iron transporters except LTCC. LTCC is upregulated by ethanol and inhibited by quercetin. In H9C2 cell, LTCC is increased by ethanol (100 mm) and/or Ang II (1 µm) concomitant with iron disorders and oxidative stress. This effect is partially normalized by quercetin (50 µm), nifedipine (LTCC inhibitor, 15 µm), or losartan (Ang II receptor antagonist, 100 µm). CONCLUSION: Alcohol-induced cardiac injury is associated with excessive NTBI uptake mediated by Ang II-LTCC activation which may be mediated by quercetin against ethanol cardiotoxicity.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180306
[Lr] Last revision date:180306
[St] Status:In-Data-Review
[do] DOI:10.1002/mnfr.201700772

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[PMID]: 29448103
[Au] Autor:Wu G; Liu Y; Liu Y; Zhang L; Zhao H; Liu L; Zhao C; Feng W
[Ad] Address:Department of Hepatology, Chongqing Three Gorges Central Hospital, Chongqing, 404000, China; Alcohol Research Center, University of Louisville School of Medicine, Louisville, KY, 40202, USA. Electronic address: wuguic@hotmail.com.
[Ti] Title:FGF 21 deficiency slows gastric emptying and reduces initial blood alcohol concentration in mice exposed to acute alcohol in fasting state.
[So] Source:Biochem Biophys Res Commun;497(1):46-50, 2018 02 26.
[Is] ISSN:1090-2104
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Excess alcohol consumption can lead to alcoholic liver disease. Fibroblast growth factor 21 (FGF21) is a metabolic regulator with multiple physiologic functions. Previous study demonstrated that FGF21 deficiency exacerbated alcohol-induced liver injury and exogenous FGF21 administration protected liver from chronic alcohol-induced injury. In this study, we aimed to explore the role of FGF21 in alcohol metabolism in mice. FGF21 knockout (KO) mice and the wild type(WT) control mice were divided into two groups and fasted for 24 h followed by a bonus of alcohol treatment at a dose of 5 g/kg body weight via gavage. Serum alcohol concentration was measured after gavage at 0.5, 2, 3, 4 and 6 h, respectively. At the end, gastric and liver tissues were collected. Serum alcohol concentration of KO mice was significantly lower than that of WT at 0.5 h after alcohol expose. There were no significant differences in alcohol dehydrogenase (ADH) activity and aldehyde dehydrogenase 2 (ALDH2) activity in gastric and liver tissues between WT and the KO mice. However, gastric emptying time of KO mice was much longer than that of WT mice. In addition, the intestinal permeability and serum GLP-1 level of KO mice were significantly higher than that of WT mice. These results suggest that FGF21 deficiency slow gastric emptying rate and indirectly influence initial alcohol metabolism in mice exposed to acute alcohol. Our findings provide additional information for understanding the gastrointestinal mechanism of alcoholic liver disease and other alcohol use disorders.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Em] Entry month:1802
[Cu] Class update date: 180303
[Lr] Last revision date:180303
[St] Status:In-Process

  3 / 3371 MEDLINE  
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[PMID]: 29286538
[Au] Autor:Sanchez-Alavez M; Wills DN; Amodeo L; Ehlers CL
[Ad] Address:Department of Neurosciences, The Scripps Research Institute, La Jolla, California.
[Ti] Title:Effect of Gabapentin on Sleep and Event-Related Oscillations (EROs) in Rats Exposed to Chronic Intermittent Ethanol Vapor and Protracted Withdrawal.
[So] Source:Alcohol Clin Exp Res;42(3):624-633, 2018 Mar.
[Is] ISSN:1530-0277
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Disturbances in sleep architecture, especially reductions in slow-wave sleep (SWS), are symptoms commonly observed in individuals with alcohol use disorders. Recent clinical trials have demonstrated that the anticonvulsant and analgesic drug gabapentin may have therapeutic value in normalizing sleep quality in recovering alcoholics. However, the brain mechanisms underlying this improvement in sleep following gabapentin treatment remain unknown. METHODS: In this study, adult Wistar rats were exposed to 8 weeks of chronic intermittent ethanol [EtOH] vapor (blood EtOH concentrations averaged 128.2 ± 17.4 mg/dl) or control conditions and then withdrawn. Sleep electroencephalograms [EEGs] and event-related oscillations (EROs) were evaluated at baseline prior to EtOH exposure and 24 hours following EtOH withdrawal. Four weeks following EtOH withdrawal the effects of saline and 2 doses of gabapentin (30, 120 mg/kg), on EROs and sleep EEGs, were evaluated. RESULTS: As compared to baseline, 24 hours following alcohol withdrawal SWS became fragmented as indexed by a significant increase in the number and a decrease in the duration of SWS episodes. Compared to controls, the EtOH-exposed group had more ERO energy in the beta frequency band in the parietal cortex. Gabapentin induced a dose-dependent decrease in the latency to the first SWS episode, and a reduction in sleep fragmentation. Gabapentin also produced a dose-dependent increase in ERO energy in the control group that was significantly attenuated in the EtOH-exposed group in the theta, and beta frequency bands. CONCLUSIONS: Taken together, these studies suggest that gabapentin can reverse some of the alcohol-induced sleep and EEG deficits but does not eliminate all of the enduring brain effects of EtOH exposure.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180304
[Lr] Last revision date:180304
[St] Status:In-Data-Review
[do] DOI:10.1111/acer.13588

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[PMID]: 29286537
[Au] Autor:Karoly HC; Bidwell LC; Mueller RL; Hutchison KE
[Ad] Address:Department of Psychology & Neuroscience , University of Colorado Boulder, Boulder, Colorado.
[Ti] Title:Investigating the Relationships Between Alcohol Consumption, Cannabis Use, and Circulating Cytokines: A Preliminary Analysis.
[So] Source:Alcohol Clin Exp Res;42(3):531-539, 2018 Mar.
[Is] ISSN:1530-0277
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: In recent years, human and animal studies have converged to support altered inflammatory signaling as a molecular mechanism underlying the pathophysiology of alcohol use disorders (AUDs). Alcohol binds to receptors on immune cells, triggering signaling pathways that produce pro-inflammatory cytokines. Chronic inflammation is associated with tissue damage, which may contribute to negative effects of AUD. Conversely, cannabis is associated with decreased inflammatory signaling, and animal studies suggest that cannabinoids may impact alcohol-induced inflammation. Thus, the impact of cannabis on inflammation in AUDs in humans warrants examination. METHODS: We explored the relationship between self-reported alcohol and cannabis use and circulating levels of the pro-inflammatory cytokines interleukin 6 (IL-6), IL-8, and IL-1ß in the blood. Among 66 regular drinkers (mean age = 30.08), we examined circulating cytokines and administered questionnaires assessing alcohol consumption and days of cannabis use over the past 90 days. We examined whether alcohol consumption, cannabis use, and gender were associated with changes in circulating cytokines, and whether there was a significant interaction between alcohol and cannabis use predicting blood levels of circulating cytokines. RESULTS: A positive association between alcohol and IL-6 emerged. We also observed a negative association between cannabis and IL-1ß. Follow-up moderation analyses indicated a cannabis by alcohol interaction predicting circulating IL-6, such that cannabis nonusers showed a stronger relationship between alcohol and IL-6 compared to cannabis users. CONCLUSIONS: These preliminary findings suggest that cannabinoid compounds may serve to mitigate inflammation associated with alcohol use. In addition, the present results provide data to inform future investigations, with the goal of ultimately leveraging knowledge of the role of inflammation in AUDs to develop more effective treatments focused on novel immune targets.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180304
[Lr] Last revision date:180304
[St] Status:In-Data-Review
[do] DOI:10.1111/acer.13592

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[PMID]: 29500720
[Au] Autor:N'Gouemo P
[Ad] Address:Department of Pediatrics, Georgetown University Medical Center, Washington, DC, USA. pn@georgetown.edu.
[Ti] Title:Voltage-Sensitive Calcium Channels in the Brain: Relevance to Alcohol Intoxication and Withdrawal.
[So] Source:Handb Exp Pharmacol;, 2018 Mar 03.
[Is] ISSN:0171-2004
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:Voltage-sensitive Ca (Ca ) channels are the primary route of depolarization-induced Ca entry in neurons and other excitable cells, leading to an increase in intracellular Ca concentration ([Ca ] ). The resulting increase in [Ca ] activates a wide range of Ca -dependent processes in neurons, including neurotransmitter release, gene transcription, activation of Ca -dependent enzymes, and activation of certain K channels and chloride channels. In addition to their key roles under physiological conditions, Ca channels are also an important target of alcohol, and alcohol-induced changes in Ca signaling can disturb neuronal homeostasis, Ca -mediated gene transcription, and the function of neuronal circuits, leading to various neurological and/or neuropsychiatric symptoms and disorders, including alcohol withdrawal induced-seizures and alcoholism.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180303
[Lr] Last revision date:180303
[St] Status:Publisher
[do] DOI:10.1007/164_2018_93

  6 / 3371 MEDLINE  
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[PMID]: 29499275
[Au] Autor:Bray JG; Reyes KC; Roberts AJ; Gruol DL
[Ad] Address:Molecular and Cellular Neuroscience Department, The Scripps Research Institute, La Jolla, CA 92037, USA.
[Ti] Title:Altered hippocampal synaptic function in transgenic mice with increased astrocyte expression of CCL2 after withdrawal from chronic alcohol.
[So] Source:Neuropharmacology;, 2018 Feb 27.
[Is] ISSN:1873-7064
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:CNS actions of the chemokine CCL2 are thought to play a role in a variety of conditions that can have detrimental consequences to CNS function, including alcohol use disorders. We used transgenic mice that express elevated levels of CCL2 in the CNS (CCL2-tg) and their non-transgenic (non-tg) littermate control mice to investigate long-term consequences of CCL2/alcohol/withdrawal interactions on hippocampal synaptic function, including excitatory synaptic transmission, somatic excitability, and synaptic plasticity. Two alcohol exposure paradigms were tested, a two-bottle choice alcohol (ethanol) drinking protocol (2BC drinking) and a chronic intermittent alcohol (ethanol) (CIE/2BC) protocol. Electrophysiological measurements of hippocampal function were made ex vivo, starting ∼0.6 months after termination of alcohol exposure. Both alcohol exposure/withdrawal paradigms resulted in CCL2-dependent interactions that altered the effects of alcohol on synaptic function. The synaptic alterations differed for the two alcohol exposure paradigms. The 2BC drinking/withdrawal treatment had no apparent long-term consequences on synaptic responses and long-term potentiation (LTP) in hippocampal slices from non-tg mice, whereas synaptic transmission was reduced but LTP was enhanced in hippocampal slices from CCL2-tg mice. In contrast, the CIE/2BC/withdrawal treatment enhanced synaptic transmission but reduced LTP in the non-tg hippocampus, whereas there were no apparent long-term consequences to synaptic transmission and LTP in hippocampus from CCL2-tg mice, although somatic excitability was enhanced. These results support the idea that alcohol-induced CCL2 production can modulate the effects of alcohol exposure/withdrawal on synaptic function and indicate that CCL2/alcohol interactions can vary depending on the alcohol exposure/withdrawal protocol used.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180302
[Lr] Last revision date:180302
[St] Status:Publisher

  7 / 3371 MEDLINE  
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[PMID]: 29492613
[Au] Autor:Thiel F; Ostafin BD; Uppendahl JR; Wichmann LJ; Schlosser M; Aan Het Rot M
[Ad] Address:Department of Psychology, University of Groningen, Grote Kruisstraat 2/1, 9712 TS, Groningen, Netherlands.
[Ti] Title:A moderate dose of alcohol selectively reduces empathic accuracy.
[So] Source:Psychopharmacology (Berl);, 2018 Feb 28.
[Is] ISSN:1432-2072
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:RATIONALE: Drinking alcohol is associated with various interpersonal effects, including effects on cognitive empathy. Empathic accuracy (EA) is a form of cognitive empathy concerned with perceivers' accuracy in inferring a target's thoughts and feelings. The effects of alcohol on EA have not previously been studied. OBJECTIVES: We examined the effect of a moderate alcohol dose on EA in social drinkers. METHODS: Fifty-four men with varying levels of hazardous drinking according to the Alcohol Use Disorders Identification Test (AUDIT) participated in a randomized, double-blind, between-group study. The alcohol group received 0.56 g/kg alcohol in a vodka and tonic-mixed drink. The placebo group received tonic, with 4 ml of vodka sprayed on top. All participants performed an EA task that involved watching 16 videos of people narrating positive and negative emotional autobiographical events and continuously rating how targets felt while narrating. RESULTS: There were no significant main effects of beverage condition on the EA task. There was an effect of the condition by AUDIT interaction for EA on the positive videos. Post-hoc simple contrasts revealed that in participants with lower AUDIT scores, the alcohol condition had lower EA for positive videos than the placebo condition. No significant main effect for condition occurred in the participants with higher AUDIT scores. CONCLUSIONS: The effect of condition in participants with lower AUDIT scores indicates alcohol selectively reduced EA in individuals low on hazardous drinking. This suggests either alcohol-induced impairments of EA for positive events or a positivity bias in men at low risk for alcohol dependency.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180301
[Lr] Last revision date:180301
[St] Status:Publisher
[do] DOI:10.1007/s00213-018-4859-y

  8 / 3371 MEDLINE  
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[PMID]: 29478745
[Au] Autor:Portero-Tresserra M; Gracia-Rubio I; Cantacorps L; Pozo OJ; Gómez-Gómez A; Pastor A; López-Arnau R; de la Torre R; Valverde O
[Ad] Address:Neurobiology of Behaviour Research Group (GReNeC-NeuroBio), Universitat Pompeu Fabra, Barcelona, Spain.
[Ti] Title:Maternal separation increases alcohol-drinking behaviour and reduces endocannabinoid levels in the mouse striatum and prefrontal cortex.
[So] Source:Eur Neuropsychopharmacol;, 2018 Feb 22.
[Is] ISSN:1873-7862
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Childhood adversity is associated with an increased risk of mood, anxiety and substance use disorders. Maternal separation is a reliable rodent model of early life adversity that leads to depression-like symptoms, which may increase the vulnerability to alcohol consumption during adolescence. However, the specific alterations in the pattern of alcohol consumption induced by maternal separation and the underlying molecular mechanisms are still unclear. The purpose of this study is to evaluate the long-term effects of maternal separation with early weaning (MSEW) on emotional and social behaviour, alcohol rewarding properties, and alcohol consumption, abstinence and relapse in adolescent male C57BL/6 mice. In addition, endocannabinoid and monoamine levels were analysed in discrete brain areas. Results showed that MSEW mice presented emotional alterations related to depressive-like behaviour and modified endocannabinoid levels in the striatum and the prefrontal cortex. MSEW mice also showed impairments in alcohol-induced conditioned place preference and higher alcohol intake in a model of binge drinking. Moreover, MSEW animals displayed a higher propensity to relapse in the two-bottle choice paradigm following a period of alcohol abstinence associated with reduced monoamine levels in the striatum. Such results indicate that exposure to early life stress increased the vulnerability to alcohol binge-drinking during adolescence, which may be partially explained by decreased sensitivity to alcohol rewarding properties and the ability to potentiate alcohol intake following a period of abstinence.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180226
[Lr] Last revision date:180226
[St] Status:Publisher

  9 / 3371 MEDLINE  
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[PMID]: 29449568
[Au] Autor:Ji Z; Yuan L; Lu X; Ding H; Luo J; Ke ZJ
[Ad] Address:Department of Biochemistry, Shanghai University of Traditional Chinese Medicine, 1200 Cailun Road, Shanghai, 201203, China.
[Ti] Title:Binge Alcohol Exposure Causes Neurobehavioral Deficits and GSK3ß Activation in the Hippocampus of Adolescent Rats.
[So] Source:Sci Rep;8(1):3088, 2018 Feb 15.
[Is] ISSN:2045-2322
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Heavy alcohol exposure causes profound damage to the adolescent brain, particularly the hippocampus, which underlie some behavioral deficits. However, the underlying molecular mechanisms remain inconclusive. The current study sought to determine whether binge alcohol exposure affects the hippocampus-related behaviors and key signaling proteins that may mediate alcohol neurotoxicity in adolescent rats. Alcohol exposure reduced the number of both NeuN-positive and doublecortin-positive cells in the hippocampus. Alcohol also induced neurodegeneration which was confirmed by ultrastructural analysis by electronic microscopy and was accompanied with the activation of microglia. Binge alcohol exposure impaired spatial learning and memory which was evaluated by the Morris water maze. However, alcohol did not alter the spontaneous locomotor activity which was determined by the open field test. GSK3ß is a multi-function serine/threonine protein kinase regulating both neuronal survival and neurogenesis and plays an important role in various neurodegenerative disorders. We have previously shown that GSK3ß is a key mediator of alcohol-induced neuron apoptosis in the developing brain. We showed here binge alcohol exposure caused GSK3ß activation by inducing dephosphorylation at Ser9 without affecting the phosphorylation of Tyr216 in the hippocampus. Thus, GSK3ß may be involved in binge alcohol exposure-induced neuronal damage to the adolescent hippocampus.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180223
[Lr] Last revision date:180223
[St] Status:In-Data-Review
[do] DOI:10.1038/s41598-018-21341-w

  10 / 3371 MEDLINE  
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[PMID]: 29463912
[Au] Autor:Domi E; Barbier E; Augier E; Augier G; Gehlert D; Barchiesi R; Thorsell A; Holm L; Heilig M
[Ad] Address:Department of Clinical and Experimental Medicine, Center for Social and Affective Neuroscience, Linköping University, Linköping, Sweden.
[Ti] Title:Preclinical evaluation of the kappa-opioid receptor antagonist CERC-501 as a candidate therapeutic for alcohol use disorders.
[So] Source:Neuropsychopharmacology;, 2018 Feb 05.
[Is] ISSN:1740-634X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Prior work suggests a role of kappa-opioid signaling in the control of alcohol drinking, in particular when drinking is escalated due to alcohol-induced long-term neuroadaptations. Here, we examined the small molecule selective kappa antagonist CERC-501 in rat models of alcohol-related behaviors, with the objective to evaluate its potential as a candidate therapeutic for alcohol use disorders. We first tested the effect of CERC-501 on acute alcohol withdrawal-induced anxiety-like behavior. CERC-501 was then tested on basal as well as escalated alcohol self-administration induced by 20% alcohol intermittent access. Finally, we determined the effects of CERC-501 on relapse to alcohol seeking triggered by both stress and alcohol-associated cues. Control experiments were performed to confirm the specificity of CERC-501 effects on alcohol-related behaviors. CERC-501 reversed anxiety-like behavior induced by alcohol withdrawal. It did not affect basal alcohol self-administration but did dose-dependently suppress self-administration that had escalated following long-term intermittent access to alcohol. CERC-501 blocked relapse to alcohol seeking induced by stress, but not when relapse-like behavior was triggered by alcohol-associated cues. The effects of CERC-501 were observed in the absence of sedative side effects and were not due to effects on alcohol metabolism. Thus, in a broad battery of preclinical alcohol models, CERC-501 has an activity profile characteristic of anti-stress compounds. Combined with its demonstrated preclinical and clinical safety profile, these data support clinical development of CERC-501 for alcohol use disorders, in particular for patients with negatively reinforced, stress-driven alcohol seeking and use.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180221
[Lr] Last revision date:180221
[St] Status:Publisher
[do] DOI:10.1038/s41386-018-0015-y


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