scholarly journals Biomarker Signatures to Monitor Alcohol Consumption and Induced Organ Damage

2021 ◽  
Author(s):  
Joy M Liji ◽  
PR Varghese ◽  
Susheela Jacobinnah ◽  
Praveenlal Kuttichira
Keyword(s):  
Sialic Acid ◽  
Alcohol Consumption ◽  
English Language ◽  
Alcohol Exposure ◽  
Organ Damage ◽  
Ethyl Esters ◽  
Total Serum ◽  
Free Access ◽  
Chronic Alcohol ◽  
Keywords Alcohol

The difficulty to differentiate long duration alcoholic behaviours is a major obstacle in the diagnosis and its treatment. Biomarkers in alcoholism are indicative of recent alcohol consumption or alcohol-induced organ damage. They are broadly divided into two; state markers, which are tools indicative of acute or chronic alcohol consumption, and trait markers, which are markers indicative of a genetic predisposition responsible to develop alcohol dependence. This review aimed to sensitise the practitioners on different alcohol state markers available now-a-days. An electronic search in Google Scholar, MEDLINE, and PubMed was conducted by using following keywords: Alcohol biomarkers, State markers, Trait markers, Alcohol consumption test. Studies on alcohol biomarkers published in English language were included in this review. Reviews and studies with free access to only abstract have been excluded. The state markers mostly used to identify chronic alcohol exposure are the Gamma-Glutamyltransferase (GGT), Aspartate and Alanine Aminotransferase (AST and ALT) which are routine serum liver function panels and Mean Corpuscular Volume (MCV) which is a haematological marker. The available non-conventional state biomarkers are Phosphatidylethanol (PEth), Fatty Acid Ethyl Esters (FAEE) and 5-Hydroxytryptophol (5-HTOL). The novel state markers which have been developed in recent research context are still awaiting validation and possible introduction to commercial settings are Plasma Sialic Acid Index of Apolipoprotein J (SIJ), Total Serum Sialic Acid (TSA), Acetaldehyde, Acetaldehyde adducts, anti-adduct antibodies and β-Hexosaminidase. Conventional alcohol biomarkers are routinely used in clinical practice. Non-conventional biomarkers seem to be promising for its estimation. Novel biomarkers are at various stages of research and development.

scholarly journals Clinical Sensitivity and Specificity of Meconium Fatty Acid Ethyl Ester, Ethyl Glucuronide, and Ethyl Sulfate for Detecting Maternal Drinking during Pregnancy

2015 ◽  
Vol 61 (3) ◽  
pp. 523-532 ◽  
Author(s):  
Sarah K Himes ◽  
Kimberly A Dukes ◽  
Tara Tripp ◽  
Julie M Petersen ◽  
Cheri Raffo ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Alcohol Consumption ◽  
Standard Condition ◽  
Acid Ethyl Ester ◽  
Alcohol Exposure ◽  
Ethyl Esters ◽  
Self Report ◽  
Ethyl Glucuronide ◽  
Ethyl Sulfate ◽  
Clinical Sensitivity

Abstract BACKGROUND We investigated agreement between self-reported prenatal alcohol exposure (PAE) and objective meconium alcohol markers to determine the optimal meconium marker and threshold for identifying PAE. METHODS Meconium fatty acid ethyl esters (FAEE), ethyl glucuronide (EtG), and ethyl sulfate (EtS) were quantified by LC-MS/MS in 0.1 g meconium from infants of Safe Passage Study participants. Detailed PAE information was collected from women with a validated timeline follow-back interview. Because meconium formation begins during weeks 12–20, maternal self-reported drinking at or beyond 19 weeks was our exposure variable. RESULTS Of 107 women, 33 reported no alcohol consumption in pregnancy, 16 stopped drinking by week 19, and 58 drank beyond 19 weeks (including 45 third-trimester drinkers). There was moderate to substantial agreement between self-reported PAE at ≥19 weeks and meconium EtG ≥30 ng/g (κ = 0.57, 95% CI 0.41–0.73). This biomarker and associated cutoff was superior to a 7 FAEE sum ≥2 nmol/g and all other individual and combination marker cutoffs. With meconium EtG ≥30 ng/g as the gold standard condition and maternal self-report at ≥19 weeks' gestation as the test condition, 82% clinical sensitivity (95% CI 71.6–92.0) and 75% specificity (95% CI 63.2–86.8) were observed. A significant dose–concentration relationship between self-reported drinks per drinking day and meconium EtG ≥30 ng/g also was observed (all P < 0.01). CONCLUSIONS Maternal alcohol consumption at ≥19 weeks was better represented by meconium EtG ≥30 ng/g than currently used FAEE cutoffs.

scholarly journals Functional Brain Networks and Alcohol Consumption: From the Naïve State to Chronic Heavy Drinking

2020 ◽  
Author(s):  
Jared A. Rowland ◽  
Jennifer R. Stapleton-Kotloski ◽  
Greg E. Alberto ◽  
April T. Davenport ◽  
Phillip M. Epperly ◽  
...  
Keyword(s):  
Alcohol Consumption ◽  
Alcohol Use ◽  
Brain Networks ◽  
Alcohol Exposure ◽  
Brain Network ◽  
Free Access ◽  
Functional Brain ◽  
Rich Club ◽  
Functional Brain Networks ◽  
The Rich

AbstractA fundamental question for alcohol use disorder is how naïve brain networks are reorganized in response to the consumption of alcohol. The current study aimed to determine the progression of alcohol’s effect on functional brain networks during the transition from naïve, to early, to chronic consumption. Resting-state brain networks of six female monkeys were acquired using magnetoencephalography prior to alcohol exposure, after early exposure, and after free-access to alcohol using a well-established model of chronic heavy alcohol use. Functional brain network metrics were derived at each time point. Assortativity, average connection frequency, and number of gamma connections changed significantly over time. All metrics remained relatively stable from naïve to early drinking, and displayed significant changes following increased quantity of alcohol consumption. The assortativity coefficient was significantly less negative (p=.043), connection frequency increased (p=.03), and gamma connections increased (p=.034). Further, brain regions considered hubs (p=.037) and members of the Rich Club (p=.012) became less common across animals following the introduction of alcohol. The minimum degree of the Rich Club prior to alcohol exposure was significantly predictive of future free-access drinking (r=-.88, p<.001). Results suggest naïve brain network characteristics may be used to predict future alcohol consumption, and that alcohol consumption alters the topology of functional brain networks, shifting hubs and Rich Club membership away from previous regions in a non-systematic manner. Further work to refine these relationships may lead to the identification of a high-risk AUD phenotype.

scholarly journals Alcohol induced hepatic retinoid depletion is associated with the induction of multiple retinoid catabolizing cytochrome P450 enzymes

PLoS ONE ◽  
2022 ◽  
Vol 17 (1) ◽  
pp. e0261675
Author(s):  
Afroza Ferdouse ◽  
Rishi R. Agrawal ◽  
Madeleine A. Gao ◽  
Hongfeng Jiang ◽  
William S. Blaner ◽  
...  
Keyword(s):  
Cytochrome P450 ◽  
Retinoic Acid ◽  
Liver Disease ◽  
Alcohol Consumption ◽  
Vitamin A ◽  
Alcohol Exposure ◽  
Chronic Alcohol ◽  
Wild Type ◽  
Chronic Alcohol Consumption ◽  
Retinyl Esters

Chronic alcohol consumption leads to a spectrum of liver disease that is associated with significant global mortality and morbidity. Alcohol is known to deplete hepatic vitamin A content, which has been linked to the pathogenesis of alcoholic liver disease. It has been suggested that induction of Cytochrome P450 2E1 (CYP2E1) contributes to alcohol-induced hepatic vitamin A depletion, but the possible contributions of other retinoid-catabolizing CYPs have not been well studied. The main objective of this study was to better understand alcohol-induced hepatic vitamin A depletion and test the hypothesis that alcohol-induced depletion of hepatic vitamin A is due to CYP-mediated oxidative catabolism. This hypothesis was tested in a mouse model of chronic alcohol consumption, including wild type and Cyp2e1 -/- mice. Our results show that chronic alcohol consumption is associated with decreased levels of hepatic retinol, retinyl esters, and retinoic acid. Moreover, the depletion of hepatic retinoid is associated with the induction of multiple retinoid catabolizing CYPs, including CYP26A1, and CYP26B1 in alcohol fed wild type mice. In Cyp2e1 -/- mice, alcohol-induced retinol decline is blunted but retinyl esters undergo a change in their acyl composition and decline upon alcohol exposure like WT mice. In conclusion, the alcohol induced decline in hepatic vitamin A content is associated with increased expression of multiple retinoid-catabolizing CYPs, including the retinoic acid specific hydroxylases CYP26A1 and CYP26B1.

scholarly journals The effect of chronic alcohol consumption on mitochondrial calcium handling in hepatocytes

2016 ◽  
Vol 473 (21) ◽  
pp. 3903-3921 ◽  
Author(s):  
Guoqiang Wang ◽  
Elisabeth Mémin ◽  
Ishwarya Murali ◽  
Lawrence D. Gaspers
Keyword(s):  
Alcohol Consumption ◽  
Alcohol Exposure ◽  
Liver Mitochondria ◽  
Calcium Handling ◽  
Chronic Alcohol ◽  
Transport Pathway ◽  
Excessive Alcohol Consumption ◽  
Intact Cells ◽  
Mitochondrial Ros ◽  
Excessive Alcohol

The damage to liver mitochondria is universally observed in both humans and animal models after excessive alcohol consumption. Acute alcohol treatment has been shown to stimulate calcium (Ca2+) release from internal stores in hepatocytes. The resultant increase in cytosolic Ca2+ is expected to be accumulated by neighboring mitochondria, which could potentially lead to mitochondrial Ca2+ overload and injury. Our data indicate that total and free mitochondrial matrix Ca2+ levels are, indeed, elevated in hepatocytes isolated from alcohol-fed rats compared with their pair-fed control littermates. In permeabilized hepatocytes, the rates of mitochondrial Ca2+ uptake were substantially increased after chronic alcohol feeding, whereas those of mitochondrial Ca2+ efflux were decreased. The changes in mitochondrial Ca2+ handling could be explained by an up-regulation of the mitochondrial Ca2+ uniporter and loss of a cyclosporin A-sensitive Ca2+ transport pathway. In intact cells, hormone-induced increases in mitochondrial Ca2+ declined at slower rates leading to more prolonged elevations of matrix Ca2+ in the alcohol-fed group compared with controls. Moreover, treatment with submaximal concentrations of Ca2+-mobilizing hormones markedly increased the levels of mitochondrial reactive oxygen species (ROS) in hepatocytes from alcohol-fed rats, but did not affect ROS levels in controls. The changes in mitochondrial Ca2+ handling are expected to buffer and attenuate cytosolic Ca2+ increases induced by acute alcohol exposure or hormone stimulation. However, these alterations in mitochondrial Ca2+ handling may also lead to Ca2+ overload during cytosolic Ca2+ increases, which may stimulate the production of mitochondrial ROS, and thus contribute to alcohol-induced liver injury.

The Association Between Alcohol Consumption and Biomarkers of Alcohol Exposure With Total Serum Immunoglobulin E Levels

2008 ◽  
Vol 32 (6) ◽  
pp. 983-990 ◽  
Author(s):  
Nele Friedrich ◽  
Lise Lotte N. Husemoen ◽  
Astrid Petersmann ◽  
Matthias Nauck ◽  
Henry Völzke ◽  
...  
Keyword(s):  
Alcohol Consumption ◽  
Immunoglobulin E ◽  
Alcohol Exposure ◽  
Serum Immunoglobulin ◽  
Total Serum

scholarly journals Transcriptome Analysis of Alcohol Drinking in Non-Dependent and Dependent Mice Following Repeated Cycles of Forced Swim Stress Exposure

2020 ◽  
Vol 10 (5) ◽  
pp. 275
Author(s):  
Sean P. Farris ◽  
Gayatri R. Tiwari ◽  
Olga Ponomareva ◽  
Marcelo F. Lopez ◽  
R. Dayne Mayfield ◽  
...  
Keyword(s):  
Alcohol Consumption ◽  
Alcohol Exposure ◽  
Maladaptive Behavior ◽  
Chronic Alcohol ◽  
Swim Stress ◽  
Forced Swim ◽  
Chronic Intermittent Ethanol ◽  
Forced Swim Stress ◽  
Chronic Alcohol Exposure ◽  
Regulated Gene Expression

Chronic stress is a known contributing factor to the development of drug and alcohol addiction. Animal models have previously shown that repeated forced swim stress promotes escalated alcohol consumption in dependent animals. To investigate the underlying molecular adaptations associated with stress and chronic alcohol exposure, RNA-sequencing and bioinformatics analyses were conducted on the prefrontal cortex (CTX) of male C57BL/6J mice that were behaviorally tested for either non-dependent alcohol consumption (CTL), chronic intermittent ethanol (CIE) vapor dependent alcohol consumption, repeated bouts of forced swim stress alone (FSS), and chronic intermittent ethanol with forced swim stress (CIE + FSS). Brain tissue from each group was collected at 0-h, 72-h, and 168-h following the final test to determine long-lasting molecular changes associated with maladaptive behavior. Our results demonstrate unique temporal patterns and persistent changes in coordinately regulated gene expression systems with respect to the tested behavioral group. For example, increased expression of genes involved in “transmitter-gated ion channel activity” was only determined for CIE + FSS. Overall, our results provide a summary of transcriptomic adaptations across time within the CTX that are relevant to understanding the neurobiology of chronic alcohol exposure and stress.

scholarly journals Rich Club Characteristics of Alcohol-Naïve Functional Brain Networks Predict Future Drinking Phenotypes in Rhesus Macaques

2021 ◽  
Vol 15 ◽  
Author(s):  
Jared A. Rowland ◽  
Jennifer R. Stapleton-Kotloski ◽  
Greg E. Alberto ◽  
April T. Davenport ◽  
Phillip M. Epperly ◽  
...  
Keyword(s):  
Alcohol Consumption ◽  
Brain Networks ◽  
Alcohol Exposure ◽  
Brain Network ◽  
Free Access ◽  
Functional Brain ◽  
Rich Club ◽  
Functional Brain Network ◽  
Functional Brain Networks ◽  
The Rich

Purpose: A fundamental question for Alcohol use disorder (AUD) is how and when naïve brain networks are reorganized in response to alcohol consumption. The current study aimed to determine the progression of alcohol’s effect on functional brain networks during transition from the naïve state to chronic consumption.Procedures: Resting-state brain networks of six female rhesus macaque (Macaca mulatta) monkeys were acquired using magnetoencephalography (MEG) prior to alcohol exposure and after free-access to alcohol using a well-established model of chronic heavy alcohol consumption. Functional brain network metrics were derived at each time point.Results: The average connection frequency (p &lt; 0.024) and membership of the Rich Club (p &lt; 0.022) changed significantly over time. Metrics describing network topology remained relatively stable from baseline to free-access drinking. The minimum degree of the Rich Club prior to alcohol exposure was significantly predictive of future free-access drinking (r = −0.88, p &lt; 0.001).Conclusions: Results suggest naïve brain network characteristics may be used to predict future alcohol consumption, and that alcohol consumption alters functional brain networks, shifting hubs and Rich Club membership away from previous regions in a non-systematic manner. Further work to refine these relationships may lead to the identification of a high-risk drinking phenotype.

scholarly journals Transcriptional Correlates of Chronic Alcohol Neuroadaptation in Drosophila Larvae

2021 ◽  
Vol 15 ◽  
Author(s):  
Amanda Anqueira-González ◽  
Jenny P. Acevedo-Gonzalez ◽  
Airined Montes-Mercado ◽  
Claudia Irizarry-Hernández ◽  
Nicolás L. Fuenzalida-Uribe ◽  
...  
Keyword(s):  
Alcohol Consumption ◽  
Conditioned Stimulus ◽  
Alcohol Exposure ◽  
Fruit Fly ◽  
Chronic Alcohol ◽  
Larval Brain ◽  
Olfactory Conditioning ◽  
Behavioral Decision ◽  
Cognitive Problems ◽  
Cellular Components

When presented with the choice, Drosophila melanogaster females will often prefer to lay eggs on food containing a significant amount of alcohol. While, in some cases, this behavioral decision can provide a survival advantage to the developing larvae, it can also lead to developmental and cognitive problems. Alcohol consumption can affect executive functions, episodic memory, and other brain function capacities. However, in the fruit fly, the initial cognitive effects of alcohol consumption have been shown to reverse upon persistent exposure to alcohol. Using an olfactory conditioning assay where an odorant is implemented as a conditioned stimulus and paired with a heat shock as an unconditioned stimulus, a previous study has shown that when exposed to a short acute dose of alcohol, Drosophila larvae can no longer learn this association. Interestingly, upon prolonged chronic alcohol exposure, larvae seem to successfully avoid the conditioned stimulus just as well as control alcohol-naive larvae, suggestive of alcohol-induced neuroadaptations. However, the mechanisms by which Drosophila adapt to the presence of alcohol remains unknown. In this study, we explore the transcriptional correlates of neuroadaptation in Drosophila larvae exposed to chronic alcohol to understand the genetic and cellular components responsible for this adaptation. For this, we employed RNA sequencing technology to evaluate differences in gene expression in the brain of larvae chronically exposed to alcohol. Our results suggest that alcohol-induced neuroadaptations are modulated by a diverse array of synaptic genes within the larval brain through a series of epigenetic modulators.

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