Castro M I, Koritnik D R, Rose J C
Endocrinology. 1986 May;118(5):1735-42. doi: 10.1210/endo-118-5-1735.
The effects of acute in utero ethanol (ETOH) treatment on basal and stimulated thyroid and insulin levels in fetal plasma were studied in chronically cannulated fetal sheep. In test situations, pregnant ewes (0.78-0.88 gestation) which were chronically cannulated received 2 g/kg ETOH [25% (vol/vol) in isotonic saline] for 2 h; this was followed by a maintenance iv infusion of 0.13 g/kg ETOH. Control animals received isovolemic infusions of isotonic saline. Fetal arterial plasma samples were obtained after the 2-h infusion, and basal levels of T3, T4, glucose, and insulin were measured. The 2-h ETOH infusion did not influence fetal basal plasma T3, T4, insulin, or glucose. Fetal thyroid responses to an intraarterial injection of 0.01, 0.10, 1.00, or 10.00 micrograms/kg TRH or of 5 mU/kg TSH through the fetal catheters were studied in the presence or absence of high plasma ETOH concentrations. Fetal T4 or T3 levels during the 4 h following any of these stimuli were not significantly different in ethanol-treated and control animals. The effects of acute ETOH exposure on insulin responses to a glucose challenge were studied in six chronically cannulated ewes and their fetuses using a cross-over experimental design. After the 2-h ETOH infusion, ewes received a bolus injection of 600 mg/kg 50% glucose, followed by a 1-h infusion of 624 mg/kg 50% glucose and 0.13 g/kg ETOH. In control situations, ewes received saline plus glucose. Acute ETOH treatment did not influence maternal or fetal plasma glucose levels at any time, but enhanced both maternal and fetal insulin responses to glucose. Total insulin release, as measured by the area under the insulin response curve, was greater during ETOH exposure in both mother (ETOH, 4740 +/- 1475 microU/ml X min; control, 2807 +/- 766 microU/ml X min; P = 0.05) and fetus (ETOH, 562 +/- 94 microU/ml X min; control, 363 +/- 46 microU/ml X min; P less than 0.05). Thus acute in utero ETOH exposure does not diminish plasma levels of either thyroid hormones or insulin, two important hormones for fetal growth and development. However, ethanol exposure enhances the insulin response to increases in blood glucose in both mother and fetus.
在长期插管的胎羊中研究了子宫内急性乙醇（ETOH）处理对胎儿血浆中基础及刺激后的甲状腺激素和胰岛素水平的影响。在测试情况下，长期插管的怀孕母羊（妊娠0.78 - 0.88）接受2 g/kg ETOH（在等渗盐水中为25%（体积/体积）），持续2小时；随后静脉维持输注0.13 g/kg ETOH。对照动物接受等体积的等渗盐水输注。在2小时输注后采集胎儿动脉血浆样本，测量T3、T4、葡萄糖和胰岛素的基础水平。2小时的ETOH输注未影响胎儿基础血浆T3、T4、胰岛素或葡萄糖水平。在存在或不存在高血浆ETOH浓度的情况下，通过胎儿导管研究了胎儿甲状腺对动脉内注射0.01、0.10、1.00或10.00微克/千克促甲状腺激素释放激素（TRH）或5 mU/千克促甲状腺激素（TSH）的反应。在这些刺激后的4小时内，乙醇处理组和对照组动物的胎儿T4或T3水平无显著差异。使用交叉实验设计在6只长期插管的母羊及其胎儿中研究了急性ETOH暴露对胰岛素对葡萄糖挑战反应的影响。在2小时的ETOH输注后，母羊接受600 mg/kg 50%葡萄糖推注，随后1小时输注624 mg/kg 50%葡萄糖和0.13 g/kg ETOH。在对照情况下，母羊接受盐水加葡萄糖。急性ETOH处理在任何时候都不影响母体或胎儿血浆葡萄糖水平，但增强了母体和胎儿对葡萄糖的胰岛素反应。通过胰岛素反应曲线下面积测量的总胰岛素释放量，在ETOH暴露期间，母体（ETOH组，4740±1475微单位/毫升×分钟；对照组，2807±766微单位/毫升×分钟；P = 0.05）和胎儿（ETOH组，562±94微单位/毫升×分钟；对照组，363±46微单位/毫升×分钟；P＜0.05）均更高。因此，子宫内急性ETOH暴露不会降低甲状腺激素或胰岛素的血浆水平，这两种激素对胎儿生长发育都很重要。然而，乙醇暴露增强了母体和胎儿对血糖升高的胰岛素反应。
