The Dwarf Mouse—An Animal with Secondary Myxedema. ∗

Abstract

Conclusion

The histological picture(2,3), low basal metabolism(5), inability of thyroid to accumulate iodine, and low PBI values shown in present study, indicate a myxedematous state in dwarf mice. Daily rat pituitary transplantations into dwarf animals restore thyroid to normal (2), from which is concluded that a pituitary factor, or factors, is responsible for the poor state of the dwarf thyroid. Thyrotropin is able to stimulate the thyroid gland of dwarf mice, and sensitivity seems greater than in normal siblings. It may be concluded that there is a lack of both thyrotropin and of somatotropin in the dwarf mouse. These mice are in a state of secondary myxedema and an important etiological factor for this disorder is thyrotropic pituitary hormone deficiency.

Summary. 1) The level of protein-bound iodine in serum of dwarf mice, determined in 2 groups of 10 each (1.2 and 1.3 g/100 ml), was very low in comparison to the value (7.3 g/100 ml) obtained on serum of 10 normal siblings. 2) Thyroids of untreated dwarf mice did not show accumulation of radioactive iodine (I¹³¹), whereas injection of thyrotropin (0.16 U.S.P.) significantly stimulated the glands to iodine uptake. 3) From these data, and previous observations, it is concluded that the dwarf mouse is a secondary myxedematous animal because of deficient production or complete lack of thyrotropic pituitary hormone.