Ekman A C, Vakkuri O, Ekman M, Leppäluoto J, Ruokonen A, Knip M
Department of Physiology, University of Oulu, Finland.
J Clin Endocrinol Metab. 1996 Jul;81(7):2627-32. doi: 10.1210/jcem.81.7.8675588.
Previous studies on the effects of ethanol on circulating pituitary hormones have been carried out mostly during daytime when the secretion of these hormones is generally at a nadir. Therefore, we studied the effects of ethanol on the nocturnal secretion of GH, PRL, TSH, and thyroid hormones (protocol I, nine healthy subjects, five women) and on the TSH and PRL responses to synthetic TRH (protocol II, healthy subjects, four women). Ethanol was given in doses of 0, 0.5 or 1.0 g/kg of BW(protocol I) and 0 or 1.0 g/kg (protocol II) and ingested po at 1900-1945 h. In protocol I, plasma GH rose from 0.6 +/- 0.2 microgram/L (mean +/- SE) at 2200 h to 25.0 +/- 4.3 micrograms/L at 0100 h in control subjects and was almost completely inhibited at 4.5 +/- 1.7 micrograms/L at 0100 h in subjects receiving 1.0 g/kg ethanol (P < 0.01). In subjects receiving 0.5 g/kg ethanol, the inhibition was also significant (P < 0.01), plasma GH being 8.2 +/- 2.5 micrograms/L at 0100 h. Plasma GHRH was measured after solid phase separation in RIA, but it did not show any ethanol-related changes. Plasma PRL exhibited a clear diurnal rhythm in control subjects and rose from 77 +/- 16 at 1800 h to 248 +/- 62 micrograms/L at 0700 h (P < 0.01). The plasma PRL profile was not affected by ethanol. Plasma TSH was 1.4 +/- 0.2 mU/L at 1800-2200 h and rose to 2.3-2.4 mU/L for 0100-0700 h (P < 0.001) in the control subjects. Ethanol 1.0 g/kg suppressed plasma TSH to 1.4 +/- 0.2 mU/L (P < 0.05 at 0100 h and P < 0.01 at 0200 h). According to the area under the curve analyses, the suppression in the nocturnal TSH was 32% in the 0.5 g/kg group and 45% in the 1.0 g/kg group (P < 0.05 for both cases). Circulating free or total T3 and T4 did not show any statistically significant changes that could explain the ethanol-induced inhibition in the nocturnal TSH peak. In protocol II, synthetic TRH (1 microgram/kg BW) was given intravenously, and blood samples were collected before, at 20 and 60 min. TRH significantly stimulated plasma TSH and PRL, but ethanol (1.0 g/kg BW) had no effect on these responses. In conclusion, small amounts of ethanol have unexpectedly great effects on nocturnal surges of TSH, and especially on those of GH, that are apparently mediated by suprapituitary mechanisms. On the other hand, ethanol did not affect the nocturnal PRL surge. These inhibitory effects of ethanol may have unfavorable effects on growth and metabolism in adolescent drinkers.
以往关于乙醇对循环垂体激素影响的研究大多是在白天进行的，而这些激素的分泌通常在白天处于最低点。因此，我们研究了乙醇对夜间生长激素（GH）、催乳素（PRL）、促甲状腺激素（TSH）和甲状腺激素分泌的影响（方案I，9名健康受试者，5名女性），以及对TSH和PRL对合成促甲状腺激素释放激素（TRH）反应的影响（方案II，健康受试者，4名女性）。乙醇的给药剂量为0、0.5或1.0 g/kg体重（方案I）以及0或1.0 g/kg（方案II），于19:00 - 19:45口服摄入。在方案I中，对照组受试者血浆GH在22:00时为0.6±0.2微克/升（均值±标准误），到01:00时升至25.0±4.3微克/升，而在接受1.0 g/kg乙醇的受试者中，01:00时几乎完全被抑制至4.5±1.7微克/升（P<0.01）。在接受0.5 g/kg乙醇的受试者中，这种抑制也很显著（P<0.01），01:00时血浆GH为8.2±2.5微克/升。采用放射免疫分析法（RIA）在固相分离后测定血浆生长激素释放激素（GHRH），但未发现与乙醇相关的变化。对照组受试者血浆PRL呈现明显的昼夜节律，在18:00时为77±16，到07:00时升至248±62微克/升（P<0.01）。血浆PRL曲线不受乙醇影响。对照组受试者血浆TSH在18:00 - 22:00时为1.4±0.2 mU/L，到01:00 - 07:00时升至2.3 - 2.4 mU/L（P<0.001）。1.0 g/kg乙醇将血浆TSH抑制至1.4±0.2 mU/L（01:00时P<0.05，02:00时P<0.01）。根据曲线下面积分析，0.5 g/kg组夜间TSH的抑制率为32%，1.0 g/kg组为45%（两种情况P均<0.05）。循环中的游离或总三碘甲状腺原氨酸（T3）和甲状腺素（T4）未显示任何具有统计学意义的变化，无法解释乙醇诱导的夜间TSH峰值抑制。在方案II中，静脉注射合成TRH（1微克/千克体重），并在注射前、20分钟和60分钟采集血样。TRH显著刺激血浆TSH和PRL，但乙醇（1.0 g/kg体重）对这些反应无影响。总之,少量乙醇对夜间TSH的激增，尤其是对GH的激增有出乎意料的巨大影响，这些影响显然是由垂体上机制介导的。另一方面，乙醇不影响夜间PRL的激增。乙醇的这些抑制作用可能对青少年饮酒者的生长和代谢产生不利影响。
