Endocrine Effects of Chronic Alcohol Abuse

Thiel, David H. Van; Gavaler, Judith S.

doi:10.1007/978-1-4757-9134-1_3

Cited by 8 publications

(6 citation statements)

References 31 publications

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“…It is known that severe alcohol consumption alters gonadal function especially when liver cirrhosis has already developed, but there is controversy regarding the pathogenesis of this alteration (34). In this study an alcohol intake .…”

Section: Discussionmentioning

confidence: 89%

Endogenous sex hormones in men aged 40-80 years

Muller

Tonkelaar

Thijssen

et al. 2003

European Journal of Endocrinology

318

241

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Objective: To determine the relationship between aging, life-style factors and health-related factors and endogenous sex hormone levels. Design: Cross-sectional study of 400 independently living men between 40 and 80 years of age. Methods: After exclusion of subjects who were not physically or mentally able to visit the study center, 400 men were randomly selected from a population-based sample. Total testosterone (TT), bioavailable testosterone (BT) (i.e. not bound to sex hormone-binding globulin (SHBG)), SHBG, estradiol (E 2 ) and dehydroepiandrosterone-sulfate (DHEA-S) were investigated for their relationship with age, body mass index (BMI), waist circumference, smoking, physical activity and general health status. Multivariate models using ANCOVA analyses were used to examine the contribution of life-style factors to sex hormone variability. Results: TT, BT and DHEA-S decreased with age; 0.2, 0.7 and 1.2%/year respectively. SHBG showed an increase with age of 1.1%/year. No changes with age were found for E 2 . General health status modified the association of TT and SHBG with age (P interaction 0.10 and 0.002 respectively). Increased BMI and waist circumference were associated with decreased TT, BT, SHBG and DHEA-S and increased E 2 (all P , 0.01). Current smoking, lower alcohol intake and a higher physical activity score were associated with higher TT and SHBG levels. Conclusion: This study showed the important determinants of sex hormones were age, BMI, waist circumference, smoking, general health status and physical activity. Furthermore, it can be concluded that general health status modified the effect between sex hormones and age. For future observational studies it should be taken into account that the above-mentioned determinants may alter the association between sex hormones and diseases and related conditions.

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Section: Discussionmentioning

confidence: 89%

Endogenous sex hormones in men aged 40-80 years

Muller

Tonkelaar

Thijssen

et al. 2003

European Journal of Endocrinology

318

241

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“…In an earlier study (Lagerspetz, 1972), shorter periods of chronic alcohol exposure (1-2 g/kg daily for 8 days) during adolescence also suppressed body weight gain. Alcohol has previously been shown to exert profound effects on various endocrine systems (Van Thiel and Gavaler, 1990; Emanuele and Emanuele, 1997). It is well-documented that growth hormone is reduced by alcohol in humans and animals (Redmond, 1981; Valimaki et al, 1990; Tentler et al, 1997; Steiner et al, 1997).…”

Section: Discussionmentioning

confidence: 99%

Chronic alcohol consumption from adolescence-to-adulthood in mice—Effect on growth and social behavior

Zou

Xie

Zhang

et al. 2009

Drug and Alcohol Dependence

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Experimentation with alcohol is common during adolescence. However the long-term consequences from moderate alcohol use during adolescence development are not clear. Using a two-bottle freechoice paradigm in the home cage setting, we studied adolescent mice (4 weeks old) across a 6-week time span of the adolescence-to-adulthood development period. Adolescent mice readily reached a steady level of alcohol consumption and maintained this level throughout the 6-week period. Chronic alcohol consumption resulted in reduced growth in adolescent mice, as well as accelerated acclimation to a novel environment. During a social interaction test, similar levels of initial social investigation and subsequent habituation were observed in both the chronic alcohol and the wateronly control groups. However, chronic alcohol self-administration resulted in impaired social recognition and decreased social play/fight behavior. Taken together, these results indicated that chronic alcohol consumption across adolescence development negatively impacted both physical growth and social behavior in mice, highlighting the detrimental consequences from prolonged alcohol drinking in adolescence.

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“…The mechanisms responsible for the intoxication, dependence, and neurotoxicity of ethanol remain largely unknown, and current data on the subject have been extensively reviewed (1)(2)(3)(4). Of the many biochemical changes that occur in the body upon ingestion of ethanol, the induction of cytochrome P450 2E1 in the liver (5) has received much attention, not only because of the capacity of this isozyme to metabolize ethanol to acetaldehyde but also because of the potential of this enzyme to cause cellular damage.…”

mentioning

confidence: 99%

Effect of ethanol on cytochrome P450 in the rat brain.

Warner

Gustafsson

1994

Proc. Natl. Acad. Sci. U.S.A.

110

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After a single dose of ethanol (0.8 ml/kg) administered intraperitoneally, the P450 content of the rat brain increased from 62 + 19 to 230 ± 97 pmol/g (wet weight) of tissue (mean ± SD, n = 5). Most of this increase could be accounted for by a 10-to 20-fold increase in the olfactory lobes and hypothalamic preoptic area. The P450s were identified by Western blot analysis and by microsequencing of the N-terminal ends after resolution of the proteins on SDS gels. They were identified as P450 2C7, 2C11, 2E1, 4A3, 4A8, and a member of the P450 2D family. In P450 extracted from the brains of control rats, P450 2C and 4A were also detectable but at a much lower concentration. P450 lA1, 2A1, 2B1, or 3A was not detected in the brains of either control or ethanol-treated rats. Oral administration of the same dose of ethanol resulted in a similar increase in the whole brain but smaller effects in the olfactory lobes. This effect of ethanol on the P450 in the brain has implications for the mechanism of toxicity and the development of tolerance to ethanol and for the effects of other drugs and environmental pollutants that act on the central nervous system.The mechanisms responsible for the intoxication, dependence, and neurotoxicity of ethanol remain largely unknown, and current data on the subject have been extensively reviewed (1-4). Of the many biochemical changes that occur in the body upon ingestion of ethanol, the induction of cytochrome P450 2E1 in the liver (5) has received much attention, not only because of the capacity of this isozyme to metabolize ethanol to acetaldehyde but also because of the potential of this enzyme to cause cellular damage. P450 2E1 can metabolically activate xenobiotics such as halothane and carbon tetrachloride to cytotoxins and nitrosamines to carcinogens (for review, see ref. 6). In addition there is a high production of oxygen radicals during its catalytic cycle, and this leads to lipid peroxidation and destruction of cell membranes (7). P450 2E1 is constitutive in the rat liver and the level ofthe protein, but not its mRNA, is increased by ethanol (8).-The enzyme is also detectable in the kidney and lung at levels that are <10% of that in the liver (9). The presence of P450 2E1 in the brain and its inducibility by ethanol is controversial. Immunohistochemical evidence indicates the presence of P450 2E1 in the brains of untreated rats in some studies (10, 11) but not in others (12), and chronic exposure of rats to ethanol in drinking water was found in one study (12) to increase the level of P450 2E1 in the brain. In the human cDNA libraries, the cDNA of P450 2E1 has been detected (13) but it is not known whether this is constitutive or due to exposure to ethanol or any of the many other organic solvents that induce this enzyme (14).The level of P450 in the brain microsomes, quantitated by its carbon monoxide difference spectrum, has been estimated in several laboratories to be 1-3% of that in the liver (15-18). We have found it impossible to measure P450 in brain microsomal fra...

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Endocrine Effects of Chronic Alcohol Abuse

Cited by 8 publications

References 31 publications

Endogenous sex hormones in men aged 40-80 years

Endogenous sex hormones in men aged 40-80 years

Chronic alcohol consumption from adolescence-to-adulthood in mice—Effect on growth and social behavior

Effect of ethanol on cytochrome P450 in the rat brain.

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