Estimation of Thyroid Gland Activity in the Snell Dwarf Mouse by Ultrastructural Observation of the Thyroid Gland, Measurement of Plasma Thyroxine Concentration and Thyroid Hormone Binding Capacity

Howe, Effie; Howe, Christopher; Pollard, Irina

doi:10.1071/bi9800471

Cited by 4 publications

(3 citation statements)

References 9 publications

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“…From 10 days of age on low thyroxine levels were linked with the appearance of dwarfism and in accordance with the hypothyroidism reported by other investigators (van Buul & Van den Brande 1978;Denef et al 1980;Howe et al 1980). The low T4 levels are accompanied by a slightly elevated T3 uptake test and a low free thyroxine index.…”

Section: Resultssupporting

confidence: 89%

Thyroxine and triiodothyronine levels in Snell mice

Buul‐Offers¹,

Hackeng²,

Schopman³

1983

Acta Endocrinologica

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Since no data are available concerning thyroid hormone levels in Snell dwarf mice from birth on, a cross-sectional study was performed of l-thyroxine (T4) and l-triiodothyronine (T3) levels in blood or serum as a function of age of several litters, starting at birth. In normal Snell mice T4 levels in blood and serum are changing with age. T4 increases during the first 2 weeks of age and declines thereafter, until adult levels of about 50 nmol/l are reached at 21 days of age. Serum T3 values are in the range of 2\p=n-\3nmol/l. They do not show such an age-related pattern. From birth on in each litter there was a clear separation between animals with low T4 levels in blood and the others. This separation was possible at all subsequent days until 9 days of age, when dwarfs can be recognized by eye. Above that age the low T4 values were associated with dwarfism. This suggests that dwarfs are hypothyroid already at birth. Serum T3 in dwarfs falls below the normal range only after 4 weeks of age, resulting in a lower T4/T3 ratio than normal.The half life time of exogenous T4 in serum of dwarfs is in the range of 13\p=n-\18h and not different from normal. For T3t\m=1/2\is 9.5\p=n-\11.1h. Dwarf mice become euthyroid by treatment with 0.1 \ g=m\ g T4 per day. 1 \ g=m\ gT4 was needed to reach a physiological level of T3. These data suggest that the peripheral conversion of T4 to T3 is slower in dwarfs than in normals. Treatment with hGH, prolactin, glucagon, insulin, testosterone and oestradiol had no influence on serum T4. As expected TSH was stimulatory.Similar results were obtained for serum T3, with the exception of prolactin which caused slightly increased levels of serum T3.The hypopituitary Snell dwarf mouse (Snell 1929) secretes very low amounts of growth hormone, prolactin and thyroid stimulating hormone

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Section: Resultssupporting

confidence: 89%

Thyroxine and triiodothyronine levels in Snell mice

Buul‐Offers¹,

Hackeng²,

Schopman³

1983

Acta Endocrinologica

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“…The deficient TSH status of the Snell mutant has been based largely on the failure to detect thyrotrophs in the anterior pituitary (Roux et al 1982), the failure of thyrotrophichormone-releasing hormone (TRH) to elicit a rise in plasma TSH (Roti, Christianson, Harris, Braverman & Vagenakis, 1978) and estimations of thyroid activity both physiologically and ultrastructurally (Howe, Howe & Pollard, 1980;Van Buul-Offers, Hackeng The exact aetiology of the condition remains unknown. Although a hypothalamic defect controlling growth-hormone production seems ruled out by the experiment of Garsner & Rennels (1960), a deficiency in hypothalamic dopamine may explain the prolactin deficiency (Morgan, Bartke & Pfeil, 1981).…”

Section: The Snell Dwarf Mousementioning

confidence: 99%

Mouse Mutants as Models in Endocrine Research

Charlton

1984

Exp Physiol

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Although Shire (1979) has listed some forty‐eight mouse mutants of interest to the endocrinologist, this short review has concentrated upon eleven mutations which have resulted in a significant number of scientific publications over the last 4 or 5 years. The selection of references has had to be limited, but it should be possible easily to expand the list given in this review. Although the proximate cause of none of the eleven mutations has been identified with certainty, the abnormalities of function have included hormone deficiencies and receptor and post‐receptor malfunctions. It is perhaps a reflexion on our society in the 1980s, that the bulk of research has concentrated on the obese mouse. However, we still do not know the initial cause of this syndrome. The major disadvantage of the mouse to the hormone assayist lies in the small blood volume and the extreme difficulty in taking serial blood samples over a short period of time. With increased sophistication of assay techniques this may prove less daunting, but is an area where a review of the literature reveals discrepancies between laboratories, and even between data generated by the same laboratory at different times. With regard to the hormone content of endocrine tissues, the way forward for peptide‐secreting glands may be in the measurement of mRNA levels for particular hormones. Certainly the methods of recombinant‐DNA technology will yield positive information upon the aetiology and expression of some of the syndromes considered above. Organ transplantation is an area in which mutant mice have proved useful, for example gonadal, pituitary and pancreatic tissue transplantation. The grafting of neural tissue in the hpg mouse has added a further dimension to this field of research. The great infrastructure of genetical research in mice has enabled us to breed mutant genes onto different genetic backgrounds. This area of research is one which deserves to expand. The techniues of in vitro fertilization, chimera formation and embryo transfer have been used, in part, in studies on mouse mutants, and should provide technical means for further investigating gene expression. The family of dwarf mutants are ideally suited for research into the expression of genes micro‐injected into the fertilized egg (see Charlton & Cox, 1983). As new hormones are isolated and become available for study these mouse mutants may well be useful in delineating physiological functions for natural and pharmacological products. Again, the dwarf mutants would seem ideally suited for research into the synthesis and action of GRF. Mouse mutants have proved of use to biochemists and embryologists and provide fertile ground for endocrine investigations ranging from molecular genetics to membrane biophysics.

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Section: The Snell Dwarf Mousementioning

confidence: 99%

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1984

Exp Physiol

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Estimation of Thyroid Gland Activity in the Snell Dwarf Mouse by Ultrastructural Observation of the Thyroid Gland, Measurement of Plasma Thyroxine Concentration and Thyroid Hormone Binding Capacity

Cited by 4 publications

References 9 publications

Thyroxine and triiodothyronine levels in Snell mice

Thyroxine and triiodothyronine levels in Snell mice

Mouse Mutants as Models in Endocrine Research

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