| First Author | Hayashi H | Year | 1995 |
| Journal | Mouse Genome | Volume | 93 |
| Issue | 1 | Pages | 151 |
| Mgi Jnum | J:24232 | Mgi Id | MGI:71981 |
| Citation | Hayashi H (1995) Aichi prefectural colony for the handicapped. Mouse Genome 93(1):151 |
| abstractText | Full text of Mouse Genome contribution: Report on a New Mutant. We have recently described a mutant mouse that is a spontaneous derivative from the Snell's Dwarf (DW/J) mouse (Yoshida et al, J. Endocrinol. 142, 435-446, 1994). It was named the growth retarded (GR) mouse" after a characteristic growth pause and delayed onset of pubertal growth. The serum T4 level of GR mice is very low and, T3 supplement advanced the onset of pubertal growth. Moreover, elevated serum TSH level that is normalized with T3 supplement, and impaired in vivo responsiveness of serum T4 to exogenous TSH were found in GR mice(Tomita et al, J. Endocrinol. in press). These results indicate that the GR mouse suffers from primary hypothyroidism. As previously known in some cases of human primary hypothyroidism, an enlargement of anterior pituitary gland that accompanies a large number of unusual hypertrophied chromophobic cells was observed in GR mice with age (Hibasami et al. BBA, 1226, 110-114, 1994). Breeding data indicated that these characteristics of the mouse inherit in an autosomal recessive manner and the gene responsible was designated "grt". Partial linkage analysis utilizing microsatellite polymorphism demonstrated that grt is not identical with lit or hyt . The GR mouse is anticipated to provide a unique animal model for the study of primary hypothyroidism and, the roles of thyroid hormones in the development and homeostasis of anterior pituitary cells as well as in the growth regulation. |
