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Publication : Stimulation of growth in the little mouse.

First Author  Beamer WH Year  1976
Journal  J Endocrinol Volume  71
Issue  1 Pages  37-45
PubMed ID  978118 Mgi Jnum  J:5710
Mgi Id  MGI:54187 Doi  10.1677/joe.0.0710037
Citation  Beamer WH, et al. (1976) Stimulation of growth in the little mouse. J Endocrinol 71(1):37-45
abstractText  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.
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