Gianoulakis C, Béliveau D, Angelogianni P, Meaney M, Thavundayil J, Tawar V, Dumas M
Douglas Hospital Research Centre, Department of Psychiatry, McGill University, Verdun, Quebec, Canada.
Life Sci. 1989;45(12):1097-109. doi: 10.1016/0024-3205(89)90167-7.
The purpose of the present studies was to investigate the activity of the adrenal gland and the pituitary beta-endorphin system in individuals from families with a 3 generation history of alcoholism, High Risk group, or from families without history of alcoholism, Low Risk group. All subjects had a medical examination, a drinking behavior personal interview and the Michigan Alcoholism Screening Test. Individuals with medical problems or excessive drinking were not included in the study. On the day of testing, a blood sample was taken at 9:00 a.m., then the subject drank a placebo drink or an ethanol solution (0.5 g ethanol/kg B.Wt.). Additional blood samples were taken at 15, 45 and 120 minutes post-drink. Results indicated that individuals of the High Risk group had lower basal levels of beta-endorphin like immunoreactivity (beta-EPLIR) than individuals of the Low Risk group. The dose of 0.5 g ethanol/kg B.Wt. induced an increase in the plasma content of beta-EPLIR of the High Risk group, but not of the Low Risk group. In the Low Risk group ethanol did not induce an increase above the 9:00 a.m. levels, however, it attenuated the beta-endorphin decrease overtime, observed following the placebo drink. Analysis of beta-endorphin-like peptides in the plasma of the High Risk group, with Sephadex G-75 chromatography indicated that the major component of the plasma beta-EPLIR was beta-lipotropin. Plasma cortisol levels, following ethanol intake, presented a small increase in the High Risk group but not in the Low Risk group. Both groups presented similar blood alcohol levels. The basal levels of immunoreactive cortisol and beta-endorphin in the plasma of individuals who were alcoholics, but had been abstinent for at least six months prior to testing were similar to the levels of the High Risk group. Thus there are differences both in the basal levels and in the response of the cortisol and the pituitary beta-endorphin system to an acute ethanol challenge between the two groups.
本研究的目的是调查有三代酗酒史的家族中的个体(高危组)以及无酗酒史的家族中的个体(低危组)的肾上腺和垂体β-内啡肽系统的活性。所有受试者均接受了医学检查、饮酒行为个人访谈以及密歇根酒精ism筛查测试。有医学问题或过度饮酒的个体未纳入研究。在测试当天,上午9:00采集血样,然后受试者饮用安慰剂饮料或乙醇溶液(0.5 g乙醇/千克体重)。在饮用后15、45和120分钟采集额外的血样。结果表明,高危组个体的β-内啡肽样免疫反应性(β-EPLIR)基础水平低于低危组个体。0.5 g乙醇/千克体重的剂量可使高危组的血浆β-EPLIR含量增加,但低危组则不然。在低危组中,乙醇并未使血浆β-EPLIR水平升高至上午9:00的水平之上,然而,它减弱了饮用安慰剂饮料后随时间观察到的β-内啡肽减少。用Sephadex G-75色谱法分析高危组血浆中的β-内啡肽样肽表明,血浆β-EPLIR的主要成分是β-促脂素。摄入乙醇后,高危组的血浆皮质醇水平略有升高,而低危组则没有。两组的血酒精水平相似。在测试前至少戒酒六个月的酗酒者血浆中免疫反应性皮质醇和β-内啡肽的基础水平与高危组相似。因此,两组在皮质醇和垂体β-内啡肽系统的基础水平以及对急性乙醇挑战的反应方面均存在差异。