ANALYSIS OF GROWTH HORMONE GENES IN MICE WITH GENETIC DEFECTS OF GROWTH HORMONE EXPRESSION

1982 ◽  
Vol 92 (3) ◽  
pp. 405-407 ◽  
Author(s):  
J. A. PHILLIPS ◽  
W. G. BEAMER ◽  
A. BARTKE
Keyword(s):  
Growth Hormone ◽  
Gh Deficiency ◽  
Genetic Disorders ◽  
Restriction Endonuclease Analysis ◽  
Genetic Defects ◽  
Ames Dwarf ◽  
Snell Dwarf ◽  
Dwarf Mice ◽  
Endonuclease Analysis ◽  
Control Litter

Restriction endonuclease analysis of genomic DNA was carried out for three types of dwarf mice (Little, Ames dwarf and Snell dwarf) that have genetic defects in GH expression. We found the GH genes to be present in homozygotes for each mutant allele as well as in their control litter-mates. These three types of dwarf mice may be useful in studying the molecular basis of inherited GH deficiency and as models for analogous genetic disorders of human GH expression.

Gonadotropin secretion, synthesis, and gene expression in human growth hormone transgenic mice and in Ames dwarf mice.

Endocrinology ◽  
1993 ◽  
Vol 132 (6) ◽  
pp. 2518-2524 ◽  
Author(s):  
K Tang ◽  
A Bartke ◽  
C S Gardiner ◽  
T E Wagner ◽  
J S Yun
Keyword(s):  
Gene Expression ◽  
Growth Hormone ◽  
Transgenic Mice ◽  
Human Growth Hormone ◽  
Human Growth ◽  
Gonadotropin Secretion ◽  
Ames Dwarf Mice ◽  
Ames Dwarf ◽  
Dwarf Mice

scholarly journals Dexamethasone Differentially Inhibits Thyroxine- or Growth Hormone-Induced Body and Organ Growth of Snell Dwarf Mice

Endocrinology ◽  
2003 ◽  
Vol 144 (6) ◽  
pp. 2553-2558 ◽  
Author(s):  
Raoul P. A. Rooman ◽  
Gilliam Kuijpers ◽  
Ria Gresnigt ◽  
Ruud Bloemen ◽  
Johanna G. Koster ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Organ Growth ◽  
Snell Dwarf ◽  
Dwarf Mice

Cellular growth in organs of dwarf mice during treatment with growth hormone, thyroxine and plasma fractions containing somatomedin activity

1982 ◽  
Vol 99 (1) ◽  
pp. 150-160 ◽  
Author(s):  
Sylvia van Buul-Offers ◽  
Jan Leo Van den Brande ◽  
L. Dumoleijn ◽  
M. Feijlbrief ◽  
C. M. Hoogerbrugge ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Human Growth ◽  
Cell Number ◽  
Small Degree ◽  
Cellular Growth ◽  
Nucleic Acid Metabolism ◽  
Plasma Fractions ◽  
Snell Dwarf ◽  
Division Cell ◽  
Dwarf Mice

Abstract. DNA, RNA and protein content of the liver, kidneys and spleen were studied in dwarf mice during treatment with human growth hormone (hGH), thyroxine and plasma fractions containing somatomedin activity (SM-P1 and SM-P4). This investigation has revealed that part of the growth of the liver and all growth of the spleen obtained with the administered preparations, are a consequence of nuclear division. Cell enlargement is not induced in the spleen by either of the preparations used. In the liver a small degree of hypertrophy is obtained with SM-P1. In the kidney both cell number and cell size are stimulated by thyroxine and to a lesser extent by hGH and SM-P1. With regards to the RNA content per cell an increase is obtained with hGH and thyroxine in the liver and in the kidneys also with SM-P1, but not in the spleen. These data demonstrate that semi-purified SM-preparations, like hGH and thyroxine, might be potent stimuli for the restoration of the impaired nucleic acid metabolism in these organs of the Snell dwarf mouse.

Pubertal development and testicular function in the male growth hormone-deficient rat

1990 ◽  
Vol 126 (2) ◽  
pp. 193-201 ◽  
Author(s):  
J. M. S. Bartlett ◽  
H. M. Charlton ◽  
I. C. A. F. Robinson ◽  
E. Nieschlag
Keyword(s):  
Gh Deficiency ◽  
Pubertal Development ◽  
Adult Life ◽  
Testicular Development ◽  
Mouse Mutants ◽  
Reproductive Axis ◽  
Snell Dwarf ◽  
Testicular Size ◽  
Sperm Output ◽  
Dwarf Mice

ABSTRACT The pubertal development of a novel GH-deficient mutant, the dwarf rat, has been evaluated. The establishment of normal spermatogenic function within small testes suggests that GH plays no role in spermatogenic function during puberty and adult life. However, a reduction in testicular size may reflect a reduced Sertoli cell population, suggesting that GH may be of importance in prepubertal testicular development. Furthermore, marked differences between the homozygous dwarf rat and homozygous GH-deficient mouse mutants (e.g. Snell, Ames, pygmy and little mutants) have been demonstrated. It would appear that the GH deficiency in the rat mutant is far more specific for GH than those hitherto described in the mouse. In contrast to Snell dwarf mice mutants, pituitary and serum concentrations of FSH and LH are normal throughout pubertal development in the dwarf rat. Both spermatogenic function and seminal vesicle function develop normally, whilst in Snell dwarf mice spermatogenic function develops late in life and seminal vesicles remain infantile. Serum and testicular concentrations of androgen are also normal in dwarf rats. Homozygous dwarf rats have been shown to be fertile in previous studies; however, our observations suggest that despite spermatogenesis being qualitatively and quantitatively normal when assessed histologically, reduced testicular size seen in dwarf rats would lead to a reduced daily sperm output in these animals. The dwarf rat represents a mutant in which the consequences of the selective depletion of GH may be studied on various endocrine systems. The reproductive axis appears to be only partially affected, at an early age, by GH deficiency. Journal of Endocrinology (1990) 126, 193–201

Effects of Spirometra erinacei plerocercoids on the growth of Snell dwarf mice

Parasitology ◽  
1983 ◽  
Vol 87 (3) ◽  
pp. 447-453 ◽  
Author(s):  
K. Shiwaku ◽  
K. Hirai ◽  
M. Torii ◽  
T. Tsuboi
Keyword(s):  
Growth Hormone ◽  
Body Weight ◽  
Body Length ◽  
Normal Male ◽  
Normal Female ◽  
Body Weights ◽  
Snell Dwarf ◽  
Spirometra Erinacei ◽  
Host Infection ◽  
Dwarf Mice

SummarySnell normal and dwarf mice were infected with Spirometra erinacei plerocercoids collected in Japan, to investigate the relationship between the growth-promoting effects of plerocercoids and the growth hormone releasing factor and the somatostatin – growth hormone – somatomedin axis in the host. Infection with plerocercoids caused increases in body weight and weights of muscle, liver, spleen and heart in the normal male mice, and increases in the head–body length, body weight and weights of muscle, liver, spleen, kidney and heart in the normal female mice, but did not increase the weight of the fat pad. Infection with plerocercoids caused increases in body weights and weights of muscle, liver and spleen in the male dwarf mice, and increases in the head–body length, body weight and weights of muscle, liver, spleen and kidney in the female dwarf mice. These observations suggest that plerocercoids promote the growth of dwarf mice as well as normal mice. As the dwarfism of Snell mice is due to a defective anterior pituitary gland, it seems that plerocercoids do not stimulate secretion of growth hormone from the pituitary. Accordingly, it seems to be more probable that the larvae secrete a growth hormone-like substance.

Growth hormone alters methionine and glutathione metabolism in Ames dwarf mice

2005 ◽  
Vol 126 (3) ◽  
pp. 389-398 ◽  
Author(s):  
Holly M. Brown-Borg ◽  
Sharlene G. Rakoczy ◽  
Eric O. Uthus
Keyword(s):  
Growth Hormone ◽  
Glutathione Metabolism ◽  
Ames Dwarf Mice ◽  
Ames Dwarf ◽  
Dwarf Mice

Changes in lymphoid organs of Ames dwarf mice after treatment with growth hormone, prolactin or ectopic pituitary transplants

1992 ◽  
Vol 15 (8) ◽  
pp. 587-595 ◽  
Author(s):  
M. A. Villanua ◽  
A. Szary ◽  
A. Bartke ◽  
A. I. Esquifino
Keyword(s):  
Growth Hormone ◽  
Lymphoid Organs ◽  
Ames Dwarf Mice ◽  
Ames Dwarf ◽  
Dwarf Mice

Body Composition of Prolactin-, Growth Hormone-, and Thyrotropin-Deficient Ames Dwarf Mice

Endocrine ◽  
2003 ◽  
Vol 20 (1-2) ◽  
pp. 149-154 ◽  
Author(s):  
Mark L. Heiman ◽  
Frank C. Tinsley ◽  
Julie A. Mattison ◽  
Steven Hauck ◽  
Andrzej Bartke
Keyword(s):  
Growth Hormone ◽  
Body Composition ◽  
Ames Dwarf Mice ◽  
Ames Dwarf ◽  
Dwarf Mice

scholarly journals Postnatal Regression of Hypothalamic Dopaminergic Neurons in Prolactin-Deficient Snell Dwarf Mice

Endocrinology ◽  
2004 ◽  
Vol 145 (12) ◽  
pp. 5656-5664 ◽  
Author(s):  
C. J. Phelps
Keyword(s):  
Neuronal Development ◽  
Cell Number ◽  
Zona Incerta ◽  
Initial Increase ◽  
Neuron Number ◽  
Ames Dwarf ◽  
Snell Dwarf ◽  
Catecholamine Fluorescence ◽  
Dwarf Mice ◽  
D 23

Abstract Both Snell (Pit-1dw or dwj, dw/dw) and Ames (Prophet of Pit-1df, df/df) dwarf mice fail to produce prolactin (PRL) as well as GH due to deficient transcription factor Pit-1 activity and have reduced numbers of hypothalamic PRL-inhibiting area A12 tuberoinfundibular dopaminergic (TIDA) neurons. It has been reported that the TIDA deficit in Ames dwarf mice develops postnatally as a reduction in number after an initial increase that is comparable to that of normal siblings. The present study was designed to characterize A12 TIDA neuronal development in the Snell dwarf (dw/dw) compared with littermate normal mice. Brains of normal (DW/?) and dwj/dwj mice were examined at 7, 14, 21, 30, and ≥ 60 postnatal days (d) by catecholamine fluorescence and quantification of neuron number after tyrosine hydroxylase immunostaining in dopaminergic (DA) areas A12, A13 (medial zona incerta), and A14 (periventricular nucleus). Fluorescence was less in dw/dw than in DW/? A12 perikarya and median eminence but was not reduced in other DA areas, such as substantia nigra, at all ages; A12 fluorescence was virtually absent in Snell dwarf adults. Numbers of TIDA neurons were comparable in normal and Snell dwarf mice at 7 d. In normal (DW/?) mice, A12 neurons increased in number to adult levels at 14 d and were significantly higher than in Snell dwarf (dw/dw) mice at 14 d (P < 0.05) and at subsequent ages (P < 0.01). In Snell dwarf mice, numbers of A12 neurons did not differ at 7, 14, and 21 d, decreased at 30 d (P < 0.05), and reached, at 60 d, 23% of the population in normal sibling mice (P < 0.01 compared with earlier ages). Neuron numbers in nonhypophysiotropic DA area A13 did not vary with age or phenotype. In A14, cell number was higher in both phenotypes at 14 d (P < 0.05 for DW/?; P < 0.01 for dw/dw); neuron number was lower in dw/dw than in DW/? mice at 30 d (P < 0.05) and 60 d (P < 0.01). Thus, compared with normal mice of the same strain, the A12 deficit is more severe in Snell (dw/dw) than in Ames (df/df) dwarf hypothalamus (48% of DF/?), as previously reported, and develops as a decline from the population present at 7 d rather than first increasing. A reduction in A14 neuron number also occurs in the Snell dwarf. Treatment of DW/dw- and dw/dw-containing litters with ovine PRL (50 μg/d, ip), beginning at 12 or 7 d and continuing until 42 d, resulted in TIDA neuron numbers in Snell dwarfs that were lower than those in normal siblings (P < 0.01 for both) but were higher than in untreated adult dwarfs and comparable to the TIDA population size in dwarfs at 7 d, indicating that PRL maintained this maximal number and prevented TIDA neuron dedifferentiation, which occurs in dwarf postnatal development.

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