Search Results
You are looking at 1 - 2 of 2 items for
- Author: T Totsuka x
- Refine by access: All content x
Search for other papers by K Tomita in
Google Scholar
PubMed
Search for other papers by T Yoshida in
Google Scholar
PubMed
Search for other papers by J Morita in
Google Scholar
PubMed
Search for other papers by S Atsumi in
Google Scholar
PubMed
Search for other papers by T Totsuka in
Google Scholar
PubMed
Abstract
The in vivo responsiveness of thyroid glands to TSH at various ages in novel 'growth-retarded' (grt/grt) mice derived from Snell's dwarf (DW/J) mice and in their normal counterparts were analysed by determining serum T4 concentrations before and after the administration of exogenous TSH. The serum T4 concentration in normal mice increased in response to TSH at 2, 4 and 12 weeks of age but not at 1 week of age. A transient augmentation of such thyroidal responsiveness to TSH was apparent in normal mice at 2 weeks of age, when the serum T4 level exhibits a peak and the pubertal growth of mice starts. In contrast to normal mice, at any age examined from 2 to 12 weeks after birth, exogenous TSH did not influence serum T4 concentrations in the grt/grt mice at all. On the other hand, serum TSH concentrations in young grt/grt mice were highly elevated compared with those in normal mice and they were normalized by a 2–3 week's treatment with T3. Morphological studies demonstrated degenerated thyroid glands in the grt/grt mice. These results suggest that the severe hypothyroidism and consequent growth retardation in growth-retarded mice are due to impairment of the thyroid glands of the mutant mice in producing and/or secreting thyroid hormones in response to TSH.
Journal of Endocrinology (1995) 144, 209–214
Search for other papers by T Yoshida in
Google Scholar
PubMed
Search for other papers by K Yamanaka in
Google Scholar
PubMed
Search for other papers by S Atsumi in
Google Scholar
PubMed
Search for other papers by H Tsumura in
Google Scholar
PubMed
Search for other papers by R Sasaki in
Google Scholar
PubMed
Search for other papers by K Tomita in
Google Scholar
PubMed
Search for other papers by E Ishikawa in
Google Scholar
PubMed
Search for other papers by H Ozawa in
Google Scholar
PubMed
Search for other papers by K Watanabe in
Google Scholar
PubMed
Search for other papers by T Totsuka in
Google Scholar
PubMed
Abstract
This paper describes a novel mutant mouse that has been spontaneously derived from the Snell's dwarf (DW/J) mouse. It was named the 'growth-retarded mouse' because of a characteristic growth pause followed by the delayed onset of pubertal growth. The onset of the increase in pituitary GH content that normally occurs concomitant with pubertal growth was also delayed in the growth-retarded mice. The serum concentration of thyroxine was very low in these mice from the neonatal period through adulthood, and a supplement of tri-iodothyronine was effective in shortening the growth pause and commencing the suppressed pubertal growth. Histological and immunohistochemical studies revealed that the anterior pituitary gland of the growth-retarded mouse contains clustered unusual chromophobic cells which are not reactive to various antisera against anterior pituitary hormones and the gland becomes enlarged with age. Breeding data indicated that these characteristics of the mice show an autosomal recessive inheritance and the gene responsible was designated as 'grm'. Partial linkage analysis utilizing microsatellite polymorphism demonstrated that the grm gene does not identify with the lit or hyt genes. Based on comparison of the hormonal status and growth pattern between growth-retarded, dwarf and normal mice, we have suggested the existence of a mutual interaction, possibly positive feedback regulation, between the pituitary and thyroid glands, that develops or matures the hormonal network which is responsible for rapid somatic growth and metabolic changes at puberty in mice.
Journal of Endocrinology (1994) 142, 435–446
