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Ethanol consumption

Ethanol is almost entirely metabolized in the liver. The first step, oxidation by alcohol dehydrogenase, yields acetaldehyde, a reactive and toxic compound. Essentially all of the acetaldehyde is converted to acetate by the liver enzyme aldehyde dehydrogenase. Aldehyde dehydrogenase is inhibited by the drag disulfiram. Given alone, disulfiram is a nontoxic substance. However, ethanol consumption in the presence of... [Pg.52]

Ethanol acts at 5-HTjg, 5-HT2C, and 5-HT3 receptors (Krystal et al. 2003b). Animal studies have shown that reduction of ethanol consumption is dependent on the presence of the 5-HT3 receptor (Hodge et al. 2004), a... [Pg.14]

Findings from animal studies suggest that neuropeptide Y (NPY) may be associated with ethanol consumption. NPY-deficient mice have increased alcohol consumption (Thiele et al. 1998), an effect that is mediated by the Y1 and Y2 receptors (Pandey et al. 2003 Thiele et al. 2000, 2002). It has been suggested that NPY Y1 agonists and Y2 antagonists may have promise in the treatment of alcoholism (Cowen et al. 2004). [Pg.15]

Thiele TE, Marsh DJ, Ste Marie L, et al Ethanol consumption and resistance are inversely related to neuropeptide Y levels. Nature 396 366-369, 1998... [Pg.53]

Another potential chnical use of GHB is in the treatment of alcohol withdrawal and alcohol dependence. In prechnical studies, GHB inhibited voluntary ethanol consumption in ethanol-preferring rats and suppressed the... [Pg.249]

Alcoholism leads to fat accumulation in the liver, hyperlipidemia, and ultimately cirrhosis. The exact mechanism of action of ethanol in the long term is stiU uncertain. Ethanol consumption over a long period leads to the accumulation of fatty acids in the liver that are derived from endogenous synthesis rather than from increased mobilization from adipose tissue. There is no impairment of hepatic synthesis of protein after ethanol ingestion. Oxidation of ethanol by alcohol dehydrogenase leads to excess production of NADH. [Pg.212]

Of the following drugs, which would not produce a syndrome of flushing, headache, nausea, vomiting, sweating, hypotension, and confusion after ethanol consumption ... [Pg.270]

Prolonged ethanol consumption accounts for 70% of all cases in the United States 10% result from other causes, and 20% are idiopathic. [Pg.322]

Jerrells, T.R. et al., Effects of ethanol consumption on mucosal and systemic T-cell-de-pendent immune responses to pathogenic microorganisms, Alcohol Clin. Exp. Res., 22 (5 Suppl), 212S, 1998. [Pg.540]

Blaha V, Yang ZJ, et al (1998) Systemic nicotine administration suppresses food intake via reduced meal sizes in both male and female rats. Acta Medica41(4) 167-173 Blanchard BA, Steindorf S, et al (1993) Sex differences in ethanol-induced dopamine release in nucleus accumbens and in ethanol consumption in rats. Alcohol Cfin Exp Res 17(5) 968-973 Booze RM, Welch MA, et al (1999) Behavioral sensitization following repeated intravenous nicotine administration gender differences and gonadal hormones. Pharmacol Biochem Behav 64(4) 827-839... [Pg.284]

Symptoms of exposure Irritates mucous membranes dermatitis with ethanol consumption flush, erythema, pruritus, urticaria, headache, nausea, vomiting, diarrhea, weakness, dizziness, difficulty in breathing. Contact with skin may cause allergic reaction (NIOSH, 1997). [Pg.1051]

Motion sickness. Effective prophylaxis can be achieved with the parasympatholytic scopolamine (p. 106) and H antihistamines (p. 114) of the diphenyl-methane type (e.g., diphenhydramine, meclizine). Antiemetic activity is not a property shared by all parasympatho-lytics or antihistamines. The efficacy of the drugs mentioned depends on the actual situation of the in vidual (gastric filling, ethanol consumption), environ-... [Pg.330]

High ethanol consumption over many years leads to liver damage. For a healthy man, the limit is about 60 g per day, and for a woman about 50 g. However, these values are strongly dependent on body weight, health status, and other factors. [Pg.320]

Mutant mice lackingNPY showincreased anxiety-relatedbehavior (Palmiter et al. 1998) a full description of the behavioral phenotype of NPY receptor-null mutant mice is not available yet. However, data from Y2 receptor-null mutants support an anti-stress activity of NPY (Tschenett et al. 2003). In addition to the anxiolytic and anti-stress effects of NPY, a relationship to alcohol intake has been described. Voluntary ethanol consumption is increased in NPY and Yi receptor-null mutant mice, whereas either NPY overexpression or potentiation of NPY signaling through blockade of Y2 receptors suppresses rodent alcohol intake (Thiel et al. 1998,2002 Thorsell et al. 2002). Thus, in addition to anxiety and depression, alcohol dependency may be a promising clinical field for newly developed NPY receptor hgands. [Pg.513]

Thiele TE, Marsh DJ, Ste Marie L, Bernstein IL, Palmiter RD (1998) Ethanol consumption and resistance are inversely related to neuropeptide Y levels. Nature 396 366-369 Thiele TE, Koh MT, Pedrazzini T (2002) Voluntary alcohol consumption is controlled via the neuropeptide Y Y1 receptor. J Neurosci 22 RC208 Thorsell A, Rimondini R, Heilig M (2002) Blockade of central neuropeptide Y (NPY) Y2 receptors reduces ethanol self-administration in rats. Neurosci Lett 332 1-4 Timmusk T, Palm K, Metsis M (1993) Multiple promoter direct tissue-specific expression of rat BDNF gene. Neuron 10 475-489... [Pg.525]

In general, ethanol in low to moderate amounts, is relatively benign to most body systems. A moderate amount of ethanol causes peripheral vasodilation, especially of cutaneous vessels, and stimulates the secretion of salivary and gastric fluids the latter action may aid digestion. On the other hand, ethanol consumption in high concentrations, as found in undiluted spirits, can induce hemorrhagic lesions in the duodenum, inhibit intestinal brush border enzymes, inhibit the uptake of amino acids, and limit the absorption of vitamins and minerals. In addition, ethanol can reduce blood testosterone levels, resulting in sexual dysfunction. [Pg.414]

A high rate of ethanol consumption can lead to inhibition of gastric secretion and irritation of the gastric mucosa. Ethanol irritates the entire gastrointestinal tract, which may lead to constipation and diminished absorption of nutrients. Other pathological effects include pancreatitis and peripheral neuropathy. Severe gonadal failure is often found in both men and women, accompanied by low blood levels of sex hormones. [Pg.415]

A variety of pathological problems involving the CNS have been described in chronic alcoholics, the main ones being Wernicke s encephalopathy and Korsakoff s psychosis Brain damage from chronic ethanol consumption can be especially severe in the elderly and may accelerate aging. [Pg.415]

Ethanol readily passes across the placenta and into the fetal circulation. The fetal alcohol syndrome has three primary features microcephaly, prenatal growth deficiency, and short palpebral fissures Other characteristics include postnatal growth deficiency, fine motor dysfunction, cardiac defects, and anomalies of the external genitalia and inner ear. A definite risk of producing fetal abnormalities occurs when ethanol consumption by the mother exceeds 3 oz daily, the equivalent of about six drinks. [Pg.415]

Volpicelli JR, Davis MA, Olgin JE. Naltrexone blocks the post-shock increase of ethanol consumption. Life Sci 1986 38 841-847. [Pg.309]

Dyr, W., W. J. McBride, T. K. Lumeng, and J. M. Murphy. 1993. "Effects of Dl and D2 Dopamine Receptor Agents on Ethanol Consumption in the High-Alcohol-Drinking (HAD) Line of Rats." Alcohol 10 207-12. [Pg.97]

A. Normal gluconeogenesis in the absence of ethanol consumption. B. Inhibition of gluconeogenesis resulting from hepatic metabolism of ethanol. [Pg.315]

There are no serious drug interactions associated with abacavir with the exception that high ethanol consumption may increase its plasma levels and affect its elimination. [Pg.183]

Rats of the Charles Foster strain were allowed to swim in a 20 cm deep plastic tub. They swam actively, paused for sometime and continued swimming. The period of immobilization with the head seldom protruded over the surface of water was recorded for each rat. The duration of immobilization is directly proportional to the depressive like state. The highly active rats are characterized by a period shorter than 130 sec and the lowly active ones by the period longer than 300 sec. It is the lowly active rats that are potential alcoholics (Paul et al., 1992). These rats were selected for tests involving ethanol consumption. In a random population of rats the... [Pg.18]


See other pages where Ethanol consumption is mentioned: [Pg.227]    [Pg.66]    [Pg.486]    [Pg.520]    [Pg.7]    [Pg.9]    [Pg.14]    [Pg.311]    [Pg.895]    [Pg.114]    [Pg.431]    [Pg.435]    [Pg.922]    [Pg.194]    [Pg.45]    [Pg.328]    [Pg.133]    [Pg.89]    [Pg.415]    [Pg.16]    [Pg.491]    [Pg.493]    [Pg.499]    [Pg.19]    [Pg.21]   
See also in sourсe #XX -- [ Pg.18 , Pg.19 , Pg.21 ]

See also in sourсe #XX -- [ Pg.611 ]




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