Faculty Research 1970 - 1979

Stimulation of growth in the little mouse.

Document Type

Article

Publication Date

1976

Keywords

Body-Weight, Bone-Lengthening, Dwarfism-Pituitary: pp, pa, Female, Male, Mice, Mice-Inbred-Strains, Mutation, Pituitary-Gland: pp, pa, tr, Pregnancy, Prolactin: df, Pseudopregnancy, Somatotropin: df, SUPPORT-U-S-GOVT-P-H-S, Transplantation-Homologous

First Page

37

Last Page

45

JAX Location

41,813

JAX Source

J-Endocrinol. 1976 Oct; 71(1):37-45.

Abstract

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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