Maly I P, Sasse D
Histochemistry. 1987;86(3):275-9. doi: 10.1007/BF00490258.
Microquantitative determinations of ADH activity were carried out on the livers of male and female rats. The animals were either starved for 84 h, or starved and then refed with a carbohydrate-rich diet for 6 nights. When the enzyme activity is expressed in mumoles/min/g dry weight, fasting does not appear to alter liver ADH activity, while in starved and subsequently refed rats it is diminished by 20%. Microquantitative measurements of ADH activity in 50-150 ng lyophilized tissue samples, microdissected the whole way along the sinusoidal length, made the computer-aided plotting of intra-acinar distribution patterns possible. The results showed that, under the feeding conditions selected, only minor changes in the ADH activity profiles occur in the liver acinus. These are within the range of the standard deviations of the normal mean values. From these results it can be deduced that fasting and refeeding do not lead to specific inhibition or induction of liver ADH activity. - The decrease of ADH activity of total liver (mumol/min) per total body weight in starved rats is obviously the result of a loss of protein which affects the liver cells of all acinar zones almost equally.
对雄性和雌性大鼠的肝脏进行了抗利尿激素（ADH）活性的微量定量测定。动物要么禁食84小时，要么禁食后再用富含碳水化合物的饮食喂养6晚。当酶活性以微摩尔/分钟/克干重表示时，禁食似乎不会改变肝脏ADH活性，而在禁食后再喂养的大鼠中，其活性降低了20%。对沿正弦长度全程显微切割的50 - 150纳克冻干组织样本中的ADH活性进行微量定量测量，使得对腺泡内分布模式进行计算机辅助绘图成为可能。结果表明，在所选择的喂养条件下，肝腺泡内的ADH活性谱仅发生微小变化。这些变化在正常平均值标准差范围内。从这些结果可以推断，禁食和再喂养不会导致肝脏ADH活性的特异性抑制或诱导。 - 饥饿大鼠中每单位总体重的全肝ADH活性（微摩尔/分钟）降低显然是蛋白质损失的结果，这种损失几乎同等程度地影响所有腺泡区的肝细胞。
