Adolescent Alcoholic Liver Disease

Taylor, Sharonda Alston; Miloh, Tamir

doi:10.1016/j.cld.2018.09.003

Cited by 9 publications

(6 citation statements)

References 8 publications

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“…According to the data of the World Health Organization (WHO) [1], one in four adolescents aged 15-19 years declares the consumption of alcoholic beverages during the previous month, while the highest number of current drinkers is recorded in European countries. Moreover, alcohol abuse accounts for around 13.5% of deaths among adolescents, indicating that it is currently becoming a serious social and health issue [1][2][3].…”

Section: Introductionmentioning

confidence: 99%

Oxidative Stress Parameters in the Liver of Growing Male Rats Receiving Various Alcoholic Beverages

et al. 2020

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Typical alcohol consumption begins in the adolescence period, increasing the risk of alcoholic liver disease (ALD) in adolescents and young adults, and while the pathophysiology of ALD is still not completely understood, it is believed that oxidative stress may be the major contributor that initiates and promotes the progression of liver damage. The aim of the present study was to assess the influence of alcohol consumption on the markers of oxidative stress and liver inflammation in the animal model of prolonged alcohol consumption in adolescents using various alcoholic beverages. In a homogenic group of 24 male Wistar rats (4 groups—6 animals per group), since 30th day of life, in order to mimic the alcohol consumption since adolescence, animals received (1) no alcoholic beverage (control group), (2) ethanol solution, (3) red wine, or (4) beer (experimental groups) for 6 weeks. Afterwards, the activities of alcohol dehydrogenase (ADH), alanine aminotransferase (ALT), and aspartate aminotransferase (AST), as well as levels of cytochrome P450-2E1 (CYP2E1), thiobarbituric acid-reactive substances (TBARS), protein carbonyl groups, tumor necrosis factor-α (TNF-α), and interleukine-10 (IL-10) were measured in liver homogenates. The difference between studied groups was observed for CYP2E1 and protein carbonyl groups levels (increased levels for animals receiving beer compared with control group), as well as for ALT activity (decreased activity for animals receiving beer compared with other experimental groups) (p < 0.05). The results suggested that some components of beer, other than ethanol, are responsible for its influence on the markers of oxidative stress and liver inflammation observed in the animal model of prolonged alcohol consumption in adolescents. Taking this into account, beer consumption in adolescents, which is a serious public health issue, should be assessed in further studies to broaden the knowledge of the progression of liver damage caused by alcohol consumption in this group.

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Section: Introductionmentioning

confidence: 99%

Oxidative Stress Parameters in the Liver of Growing Male Rats Receiving Various Alcoholic Beverages

et al. 2020

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“…The WHO estimates 16% of drinkers worldwide engage in heavy episodic drinking and 7.5% have at least one heavy drinking episode per month [21]. The risk of alcohol dependence increases based on genetic and psychosocial factors [11].…”

Section: Alcohol Consumption and Related Liver Diseasesmentioning

confidence: 99%

Alcohol Induced Fatty Liver: A Tragic Inception of Wrong Turn

2019

ARC Journal of Nursing and Healthcare

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Alcohol is a noteworthy reason for liver cirrhosis in the Western world and records for most of instances of liver cirrhosis found in region general emergency clinics in the UK. Alcoholic liver disease is a term that incorporates the liver appearances of alcohol overconsumption, including fatty liver, alcoholic hepatitis, and constant hepatitis with liver fibrosis or cirrhosis. As per the American Liver Foundation (ALF), somewhere in the range of 10 and 20 percent of substantial consumers will develop cirrhosis. The disease is a piece of a progression. It might begin with fatty liver disease, at that point advancement to alcoholic hepatitis, and after that to alcoholic cirrhosis. Be that as it may, it's conceivable an individual can develop alcoholic liver cirrhosis while never having alcoholic hepatitis. Symptoms of alcoholic liver cirrhosis regularly develop when an individual is between the ages of 30 and 40. All things considered, it takes around one hour for the body to utilize (separate) one standard beverage as characterized by U.S. rules (for example 12 ounces of 4.5% brew, 5 ounces of 11% wine, or 1.5 ounces of 35% alcohol). Utilization of 60-80g every day (14g is viewed as one standard beverage in the US, i.e., 1.5 fl oz hard alcohol, 5 fl oz wine, 12 fl oz lager; drinking a six-pack of brew day by day would be amidst the range) for a long time or more in men, or 20g/day for ladies fundamentally builds the danger of hepatitis and fibrosis by 7% to 47%. Of all endless substantial consumers, just 15-20% develop hepatitis or cirrhosis, which can happen correspondingly or in progression. The purpose for is accepted to be the liver has gigantic ability to recover and notwithstanding when 75% of hepatocytes are dead, it keeps on working as should be expected. As indicated by NIAAA (1993), somewhere in the range of 10% and 35% of substantial consumers develop alcoholic hepatitis. While development of hepatitis isn't specifically identified with the portion of alcohol, a few people appear to be more prone to this response than others. This is called alcoholic steato-necrosis (Steatosis) and the inflammation seems to incline to liver fibrosis.

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“…Adolescence is a complex period, which involves many different hormonal pathways that orchestrate physical and biological changes, encompassing increased growth and metabolic rate, alterations in fat and muscle, and breast and genital development (Khan, 2019; Vijayakumar et al., 2018). In this context, BD consumption during adolescence has recently been associated with hepatic damage (Taylor & Miloh, 2019), increased heart rate (Ojeda et al., 2021; Ramírez‐Piña et al., 2021), reduced microvasculature function (Bian et al., 2018), kidney ionic imbalance (Sobrino et al., 2019) and even insulin disturbances (Steiner & Lang, 2017), which are situations that predispose adolescents to future adult cardiometabolic problems (Ojeda et al., 2022). Furthermore, the adolescent heart is substantially more sensitive to these effects than the adult one (Ai et al., 2020).…”

Section: Introductionmentioning

confidence: 99%

Adipose tissue homeostasis orchestrates the oxidative, energetic, metabolic and endocrine disruption induced by binge drinking in adolescent rats

Romero‐Herrera,

Nogales,

Gallego‐López

et al. 2023

The Journal of Physiology

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Binge drinking (BD) is the most common alcohol consumption model for adolescents, and has recently been related to the generation of high oxidation and insulin resistance (IR). White adipose tissue (WAT) is a target organ for insulin action that regulates whole‐body metabolism by secreting adipokines. The present study aimed to analyse the oxidative, inflammatory, energetic and endocrine profile in the WAT of BD‐exposed adolescent rats, to obtain an integrative view of insulin secretion and WAT in IR progression. Two groups of male adolescent rats were used: control (n = 8) and BD (n = 8). An intermittent i.p. BD model (20% v/v) was used during 3 consecutive weeks. BD exposure led to a pancreatic oxidative imbalance, which was joint to high insulin secretion by augmenting deacetylase sirtuin‐1 (SIRT‐1) pancreatic expression and serum adipsin levels. However, BD rats had hyperglycaemia and high homeostasis model assessment of insulin resistance value (HOMA‐IR). BD exposure in WAT increased lipid oxidation, as well as decreased insulin receptor substrate 1 (IRS‐1) and AKT expression, sterol regulatory element‐binding protein 1 (SREBP1), forkhead box O3A (FOXO3a) and peroxisome proliferator‐activated receptor γ (PPARγ), and adipocyte size. BD also affected the expression of proteins related to energy balance, such as SIRT‐1 and AMP activated protein kinase (AMPK), affecting the adipokine secretion profile (increasing resistin/adiponectin ratio). BD altered the entire serum lipid profile, increasing the concentration of free fatty acids. In conclusion, BD led to an oxidative imbalance and IR process in WAT, which modified the energy balance in this tissue, decreasing the WAT lipogenic/lipolytic ratio, affecting adipokine secretion and the systemic lipid profile, and contributing to the progression of IR. Therefore, WAT is key in the generation of metabolic and endocrine disruption after BD exposure during adolescence in rats. imageKey points Adolescent rat binge drinking (BD) exposure leads to hepatic and systemic oxidative stress (OS) via reactive oxygen species generation, causing hepatic insulin resistance (IR) and altered energy metabolism. In the present study, BD exposure in adolescent rats induces OS in the pancreas, with increased insulin secretion despite hyperglycaemia, indicating a role for IR in white adipose tissue (WAT) homeostasis. In WAT, BD produces IR and an oxidative and energetic imbalance, triggering an intense lipolysis where the serum lipid profile is altered and free fatty acids are increased, consistent with liver lipid accumulation and steatosis. BD exposure heightens inflammation in WAT, elevating pro‐inflammatory and reducing anti‐inflammatory adipokines, favouring cardiovascular damage. This research provides a comprehensive view of how adolescent BD in rats impacts liver, WAT and pancreas homeostasis, posing a risk for future cardiometabolic complications in adulthood.

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Adolescent Alcoholic Liver Disease

Cited by 9 publications

References 8 publications

Oxidative Stress Parameters in the Liver of Growing Male Rats Receiving Various Alcoholic Beverages

Oxidative Stress Parameters in the Liver of Growing Male Rats Receiving Various Alcoholic Beverages

Alcohol Induced Fatty Liver: A Tragic Inception of Wrong Turn

Adipose tissue homeostasis orchestrates the oxidative, energetic, metabolic and endocrine disruption induced by binge drinking in adolescent rats

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