Increased alcohol intake in low alcohol drinking rats after chronic infusion of the β-carboline harman into the hippocampus

1994 ◽  
Vol 49 (4) ◽  
pp. 949-953 ◽  
Author(s):  
Albert Adell ◽  
R.D. Myers
Keyword(s):  
Alcohol Drinking ◽  
Alcohol Intake ◽  
Chronic Infusion ◽  
Low Alcohol

scholarly journals Moderate alcohol intake promotes pancreatic ductal adenocarcinoma development in mice expressing oncogenic Kras

2020 ◽  
Vol 318 (2) ◽  
pp. G265-G276
Author(s):  
Kinji Asahina ◽  
Steven Balog ◽  
Edward Hwang ◽  
Eugene Moon ◽  
Emily Wan ◽  
...  
Keyword(s):  
Risk Factors ◽  
Risk Factor ◽  
Pancreatic Ductal Adenocarcinoma ◽  
Alcohol Drinking ◽  
Calcium Binding ◽  
Alcohol Intake ◽  
Western Diet ◽  
Mutant Mice ◽  
Ductal Adenocarcinoma ◽  
Moderate Alcohol Intake

Kras mutations are associated with pancreatic ductal adenocarcinoma (PDAC). Although tobacco smoking, pancreatitis, and obesity are known environmental risk factors for PDAC, the contribution of moderate alcohol intake to PDAC remains elusive. In the present study, we tested whether a combination of risk factors or moderate alcohol intake induces PDAC development in mice. Control Pdx1Cre and Pdx1Cre;LSL- KrasG12D mutant mice were fed a Western alcohol diet containing high levels of cholesterol and saturated fat, 3.5% alcohol, and lipopolysaccharide for 5 mo. In addition, mice were treated with cerulein, for induction of pancreatitis, and nicotine every month. Treatment with all of these risk factors promoted development of advanced pancreatic neoplasia and PDAC in the Pdx1Cre;LSL- KrasG12D mice but not in the control Pdx1Cre mice. Moderate alcohol intake or Western diet feeding also significantly promoted advanced neoplasia and PDAC development in Pdx1Cre;LSL- KrasG12D mice compared with mice fed a regular chow. Alcohol, but not Western diet, increased tumor development in the liver in the Pdx1Cre;LSL- KrasG12D mice, but its origin remained elusive due to leakiness of Pdx1Cre in hepatocytes. RNA-seq analysis revealed that alcohol feeding increases expression of markers for tumors ( Epcam, Krt19, Prom1, Wt1, and Wwtr1), stroma ( Dcn, Fn1, and Tnc), and cytokines ( Tgfb1 and Tnf) and decreases expression of Fgf21 and Il6 in the pancreatic tumor tissues. Immunostaining showed heterogeneous expression of nephronectin, S100 calcium-binding protein A6, and vascular cell adhesion molecule 1 in pancreatic tumors surrounded by podoplanin-positive stromal cells. Our data indicate that moderate alcohol drinking is a risk factor for development of PDAC. NEW & NOTEWORTHY Heavy alcohol intake has been suspected to be a risk factor of pancreatic ductal adenocarcinoma (PDAC) in humans. However, the contribution of moderate alcohol intake to PDAC development remains elusive. In the present study, we experimentally show that moderate alcohol feeding significantly induces advanced stages of pancreatic intraepithelial neoplasia development and invasive PDAC in Pdx1Cre;LSL- KrasG12D mutant mice. Our data indicate that moderate alcohol drinking is a risk factor for PDAC.

Effects of Stress on Alcohol Consumption in Rats Selectively Bred for High or Low Alcohol Drinking

2004 ◽  
Vol 28 (3) ◽  
pp. 385-393 ◽  
Author(s):  
Julia A. Chester ◽  
Annette M. Blose ◽  
Mark Zweifel ◽  
Janice C. Froehlich
Keyword(s):  
Alcohol Consumption ◽  
Alcohol Drinking ◽  
Effects Of Stress ◽  
Low Alcohol

Ethanol effects on local cerebral glucose utilization in high-alcohol-drinking and low-alcohol-drinking rats

Alcohol ◽  
2003 ◽  
Vol 29 (1) ◽  
pp. 1-9 ◽  
Author(s):  
Jennifer E Learn ◽  
Daniel G Smith ◽  
William J McBride ◽  
Lawrence Lumeng ◽  
Ting-Kai Li
Keyword(s):  
Alcohol Drinking ◽  
Glucose Utilization ◽  
High Alcohol ◽  
Local Cerebral Glucose Utilization ◽  
Cerebral Glucose Utilization ◽  
Low Alcohol

Abstract P158: Systematic Review and Meta-analysis of Acute Effects of Alcohol Consumption on Risk of Cardiovascular Events

Circulation ◽  
2016 ◽  
Vol 133 (suppl_1) ◽  
Author(s):  
Elizabeth Mostofsky ◽  
Harpreet S Chahal ◽  
Kenneth J Mukamal ◽  
Eric B Rimm ◽  
Murray A Mittleman
Keyword(s):  
Cardiovascular Risk ◽  
Alcohol Consumption ◽  
Alcohol Drinking ◽  
Lower Risk ◽  
Cardiovascular Events ◽  
Alcohol Intake ◽  
Meta Analysis ◽  
Moderate Alcohol Consumption ◽  
Consistent Finding ◽  
Heavy Alcohol

Introduction: Although considerable research describes the cardiovascular effects of habitual moderate and heavy alcohol consumption, the acute risks following alcohol intake have not been well characterized. Based on its physiological effects, alcohol may have markedly different effects on acute and long-term risk. We assessed the hypothesis that moderate alcohol consumption is associated with an immediately higher risk of cardiovascular events that becomes protective after 24 hours, whereas heavy alcohol drinking is associated with higher cardiovascular risk both immediately and in the following days. Methods: We searched CINAHL, Embase, PubMed and PsycINFO from inception to March 12 2015, supplemented with manual screening for observational studies assessing the association between alcohol intake and cardiovascular events in the following hours and days. We calculated pooled relative risks (RRs) and 95% confidence intervals (CIs) for the association between alcohol intake and myocardial infarction (MI), ischemic stroke (IS) and hemorrhagic stroke (HS) using DerSimonian and Laird random-effects models to model any alcohol intake or dose-response relationships of alcohol intake and cardiovascular events. Results: Among 1056 citations and 37 full-text articles reviewed, 23 studies (29457 participants) were included. Moderate alcohol consumption was associated with an acutely higher cardiovascular risk that was attenuated after 24 hours and even protective for MI and HS (≈2-4 drinks: RR=30% lower risk), and protective against IS within one week (≈6 drinks: RR=19% lower risk). In contrast, heavy alcohol drinking was associated with higher cardiovascular risk in the following day (≈6-9 drinks: RR=1.3-2.3) and week (≈19-30 drinks: RR=2.25-6.2). Conclusions: In conclusion, there appears to be a consistent finding of an acutely higher cardiovascular risk following any alcohol consumption but by 24 hours, only heavy alcohol intake conferred continued risk.

scholarly journals Behavioral and Neurobiological Consequences of Hedonic Feeding on Alcohol Drinking

2020 ◽  
Vol 26 (20) ◽  
pp. 2309-2315 ◽  
Author(s):  
Julianna Brutman ◽  
Jon F. Davis ◽  
Sunil Sirohi
Keyword(s):  
Alcohol Drinking ◽  
Alcohol Intake ◽  
Energy Homeostasis ◽  
Drugs Of Abuse ◽  
Drinking Behavior ◽  
The Body ◽  
Alcohol And Drugs ◽  
Signaling Mechanisms ◽  
Functional Consequences ◽  
Neuropsychiatric Conditions

A complex interplay of peripheral and central signaling mechanisms within the body of an organism maintains energy homeostasis. In addition, energy/food intake is modified by various external factors (e.g., palatability, food availability, social and environmental triggers). Highly palatable foods can provoke maladaptive feeding behavior, which in turn disrupts normal homeostatic regulation resulting in numerous health consequences. Furthermore, neuroendocrine peptides, traditionally considered to regulate appetite and energy homeostasis, also control the intake and reinforcing properties of alcohol and drugs of abuse. Therefore, dysregulated eating as a result of a hedonic/binge-like intake of hyper-palatable food may impact alcohol drinking behavior. Relevant in this case is the fact that eating disorders are highly comorbid with several neuropsychiatric conditions, including alcohol use disorder. The present review is intended to summarize the neurobiological and functional consequences of hedonic feeding on alcohol intake.

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