Moderate alcohol drinking: Effects on the heart and liver

Brenner, David A.

doi:10.1053/gast.2000.20206

Cited by 7 publications

(5 citation statements)

References 21 publications

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“…The problems of acute intoxication, dependence and withdrawal, and deaths associated with stroke, alcoholic cirrhosis, road injury, and suicide are problems with which we, as physicians, are all too familiar (31). The effects of alcohol consumption follow a U‐ or J‐shaped curve, with important benefits for light‐to‐moderate consumption but with increased risk at high levels of consumption (32, 33).…”

Section: Discussionmentioning

confidence: 99%

Alcohol Consumption in the Severely Obese: Relationship with the Metabolic Syndrome

Dixon

O'Brien

2002

Obesity Research

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DIXON, JOHN B., MAUREEN E. DIXON, AND PAUL E. O'BRIEN. Alcohol consumption in the severely obese: relationship with the metabolic syndrome. Obes Res. 2002; 10:245-252. Objective: The aim of this study was to examine the association between the clinical and biochemical features of the metabolic syndrome and quantity and type of alcohol intake in the severely obese. Research Methods and Procedures:A cross-sectional study was performed in 486 consecutive severely obese subjects. Data on alcohol consumption was collected by serial clinical interviews and a questionnaire. The relationship between alcohol intake and the clinical and serum chemistry features of the metabolic syndrome was analyzed by multiple statistical techniques. Laboratory measures included lipid profile, fasting blood glucose, hemoglobin A1c, and fasting serum insulin. An indirect index of insulin resistance was calculated using the log-transformed fasting insulin and glucose product. Results: There were 486 subjects, 84% women, with a mean age of 40.6 Ϯ 10 years (range, 16 to 71 years) and a body mass index of 45.3 Ϯ 7 kg/m 2 (range, 34 to 77 kg/m 2 ). Alcohol consumers (N ϭ 276) showed a marked reduction in the adjusted odds ratio of type 2 diabetes (odds ratio ϭ 0.29; 95% confidence interval, 0.16 to 0.55) compared with rare or nonconsumers (N ϭ 210). There was a U-shaped relationship between the amount and frequency of alcohol consumption and fasting triglyceride, fasting glucose, hemoglobin A1c, and index of insulin resistance measurements. Consumers of Ͻ100 g/wk had more favorable measures. The effect was attenuated when diabetics were excluded from the analysis. Timing of alcohol consumption did not influence outcome measures.Discussion: Light-to-moderate alcohol consumption is associated with a lower prevalence of type 2 diabetes, reduced insulin resistance, and more favorable vascular risk profile in the severely obese. We would propose that light to moderate alcohol consumption should not be discouraged in the severely obese.

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Section: Discussionmentioning

confidence: 99%

Alcohol Consumption in the Severely Obese: Relationship with the Metabolic Syndrome

Dixon

O'Brien

2002

Obesity Research

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“…Several epidemiological studies have reported an association between regular light-to-moderate ethanol consumption and lower risk of mortality and morbidity from life-threatening diseases (13)(14)(15)(16)(17)(18). It has been shown that light-to-moderate ethanol consumption is associated with lower risk of development of insulin resistance (19,20) and type 2 diabetes (21) and protection against the risk of major cardiovascular disease events such as myocardial infarction and coronary artery disease in healthy populations (22,23) and in patients with type 2 diabetes (24,25), hypertension (26,27) and myocardial infarction (28,29).…”

Section: Introductionmentioning

confidence: 99%

Light-to-Moderate Ethanol Feeding Augments AMPK-α Phosphorylation and Attenuates SREBP-1 Expression in the Liver of Rats

Nammi

Roufogalis

2013

J Pharm Pharm Sci

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Purpose: Fatty liver disease, a hepatic manifestation of metabolic syndrome, is one of the major causes of chronic liver diseases. Epidemiological studies suggest that regular light-to-moderate ethanol consumption lowers the risk of developing metabolic disorders including dislipidemia, insulin resistance, type 2 diabetes and fatty liver disease. However, the mechanism(s) of the protective effect of light-to-moderate ethanol consumption on the liver remains unknown. Methods: In the present study, we investigated the effects of light (6%, 0.94 g/kg/day) and moderate (12%, 1.88 g/kg/day) ethanol feeding in rats for 3 weeks on the circulating and hepatic biochemical profiles and on the hepatic protein expression and phosphorylation status of adenosine monophosphate-activated protein kinase-α (AMPK-α) and other down-stream targets of this enzyme including sterol regulatory element-binding protein-1 (SREBP-1), SREBP cleavage-activating protein (SCAP) and 3-hydroxy-3-methyl-glutaryl-CoA reductase (HMG-CoA reductase). Results: Despite no significant difference in food-intake among the groups, light ethanol treatment significantly increased the body weight compared to control rats. Serum glucose, insulin, total cholesterol, triglycerides, phospholipids and hepatic cholesterol and triglycerides were not significantly different among the groups. However, serum free fatty acids were significantly reduced with light ethanol treatment. Both light and moderate ethanol treatment significantly increased the hepatic levels of phosphorylated AMPK-α protein and this was associated with significant reduction of SREBP-1 protein expression, suggesting an enhanced fatty acid oxidation. In addition, light ethanol treatment significantly decreased the SCAP protein expression in the liver. However, liver HMG-CoA protein expression was not significantly different with ethanol consumption. Conclusion: Chronic light-to-moderate ethanol consumption increased AMPK activation which was associated with decreased expression of SREBP-1 and SCAP in the liver. Thus, our studies provide mechanistic evidence for the earlier epidemiological studies that indicate light-to-moderate ethanol intake lowers the risk of development of fatty liver disease and other metabolic disorders. Our studies demonstrate that the protective effects of light-to-moderate ethanol arise at least in part by increased phosphorylation of AMPK-α and decreased SREBP-1 expression in the liver. Further studies are warranted to determine the effects of light-to-moderate ethanol on intracellular up-stream and down-stream targets of AMPK and also on the implications of light-to-moderate ethanol in protecting non-alcoholic fatty liver disease. This article is open to POST-PUBLICATION REVIEW. Registered readers (see “For Readers”) may comment by clicking on ABSTRACT on the issue’s contents page.

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“…However, most alcohol-associated diseases occur in a dose-dependent manner. Moderate alcohol drinking can reduce the risk of many diseases 4 5 : the generation and development of insulin resistance and type 2 diabetes 6 7 , dementia, cognitive disorders, osteoporosis and cancer 8 9 10 . In addition, moderate drinking can also prevent the occurrence of major cardiovascular disease 11 12 .…”

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confidence: 99%

Chronic Moderate Alcohol Intakes Accelerate SR-B1 Mediated Reverse Cholesterol Transport

Diao

Liu

et al. 2016

Sci Rep

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Cholesterol is essential for all animal life. However, a high level of cholesterol in the body is strongly associated with the progression of various severe diseases. In our study, the potential involvement of alcohol in the regulation of high density lipoprotein (HDL) receptor scavenger receptor class B and type I (SR-B1)-mediated reverse cholesterol transport was investigated. We separated male C57BL/6 mice into four diets: control, alcohol, Control + HC and alcohol + HC. The SR-B1 level and 1,1′-dioctadecyl-3,3,3′,3′-tetramethylindocarbocyanine perchlorate- high- density lipoprotein (DiI-HDL) uptake were also measured in AML12 cells and HL7702 cells treated with alcohol. The control + HC diet led to increased hepatic triglyceride and cholesterol levels while alcohol + HC led no significant change. Compared with that of the control group, the SR-B1 mRNA level was elevated by 27.1% (P < 0.05), 123.8% (P < 0.001) and 343.6% (P < 0.001) in the alcohol, control + HC and alcohol + HC groups, respectively. In AML12 and HL7702 cells, SR-B1 level and DiI-HDL uptake were repressed by SR-B1 siRNA or GW9662. However, these effects were reversed through alcohol treatment. These data suggest that a moderate amount of alcohol plays a novel role in reverse cholesterol transport, mainly mediated by PPARγ and SR-B1.

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Moderate alcohol drinking: Effects on the heart and liver

Cited by 7 publications

References 21 publications

Alcohol Consumption in the Severely Obese: Relationship with the Metabolic Syndrome

Alcohol Consumption in the Severely Obese: Relationship with the Metabolic Syndrome

Light-to-Moderate Ethanol Feeding Augments AMPK-α Phosphorylation and Attenuates SREBP-1 Expression in the Liver of Rats

Chronic Moderate Alcohol Intakes Accelerate SR-B1 Mediated Reverse Cholesterol Transport

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