Beamer W H, Eicher E M
J Endocrinol. 1976 Oct;71(1):37-45. doi: 10.1677/joe.0.0710037.
The new mouse mutation little (lit) in the homozygous state causes a pituitary deficiency involving at least growth hormone (GH) and prolactin. The resultant growth failure of lit/lit mice was shown to be reversed by experimental conditions that enhanced levels of GH or GH and prolactin in the circulation. Two measures of growth, actual weight gain and bone dimension, were significantly improved by the physiological processes of pregnancy and pseudopregnancy, by extra-sellar graft of a normal mouse pituitary, and by treatment with GH but not prolactin. These data confirmed pituitary dysfunction as the basic defect caused by the mutation lit and showed that the GH deficiency is responsible for growth failure. However, the biological site of gene action, the pituitary or hypothalamus, has not been established. Little mice exhibit a number of characteristics similar to those of human genetic ateleotic dwarfism Type 1, namely genetic inheritance, time of onset of growth retardation, proportionate skeletal size reduction, and pituitary GH deficiency.
纯合状态下的新小鼠突变体“矮小”（lit）会导致垂体功能缺陷，至少涉及生长激素（GH）和催乳素。实验条件下，循环中GH水平或GH与催乳素水平升高可逆转lit/lit小鼠由此产生的生长衰竭。怀孕和假孕的生理过程、正常小鼠垂体的鞍外移植以及GH而非催乳素治疗，显著改善了生长的两项指标，即实际体重增加和骨骼尺寸。这些数据证实垂体功能障碍是由lit突变引起的基本缺陷，并表明GH缺乏是生长衰竭的原因。然而，基因作用的生物学位点，即垂体还是下丘脑，尚未确定。矮小小鼠表现出许多与人类遗传性1型非典型性侏儒症相似的特征，即遗传方式、生长迟缓的起始时间、骨骼大小成比例减小以及垂体GH缺乏。
