STIMULATION OF GROWTH IN LITTLE MOUSE
STIMULATION OF GROWTH IN LITTLE MOUSE
复制标题
DOI：
10.1677/joe.0.0710037
复制
发表时间：
1976-01-01
影响因子：
4
通讯作者：
EICHER, EM
中科院分区：
文献类型：
--
作者：
BEAMER, WG;EICHER, EM
纯合子状态下新的小鼠突变little （lit）导致至少涉及生长激素（GH）和催乳素的垂体缺陷。通过提高循环中生长激素或生长激素和催乳素水平的实验条件，可以逆转lit/lit小鼠的生长衰竭。通过妊娠和假妊娠的生理过程、经鞍外移植的正常小鼠垂体以及用生长激素而非催乳素治疗，两项生长指标——实际体重增加和骨尺寸显著改善。垂体功能障碍是由突变引起的基本缺陷，生长激素缺乏是导致生长失败的原因。基因作用的生物学位点，垂体或下丘脑，尚未确定。小白鼠表现出许多与人类1型遗传性失步性侏儒症相似的特征，即遗传遗传、生长发育迟缓的发病时间、相应的骨骼大小缩小和垂体GH缺乏。
The new mouse mutation little (lit) in the homozygous state causes a pituitary deficiency involving at least growth hormone (GH) and prolactin. The reultant growth failure of lit/lit mice was 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. Pituitary dysfunction is the basic defect caused by the mutation lit and the GH deficiency is responsible for growth failure. The biological site of gene action, the pituitary or hypothalamus, was not established. Little mice exhibit a number of characteristics similar to those of human genetic atelegtic dwarfism Type 1, namely genetic inheritance, time of onset of growth retardation, proportionate skeletal size reduction, and pituitary GH deficiency.