Prolactin Induces Tuberoinfundibular Dopaminergic Neurone Differentiation in Snell Dwarf Mice if Administered Beginning at 3 Days of Age

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.

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Testicular growth and hormonal parameters in the male Snell dwarf mouse

Acta Endocrinologica ◽

10.1530/acta.0.1150399 ◽

1987 ◽

Vol 115 (3) ◽

pp. 399-405 ◽

Cited By ~ 8

Author(s):

M. T. Hochereau-de Reviers ◽

M. M. de Reviers ◽

C. Monet-Kuntz ◽

C. Perreau ◽

I. Fontaine ◽

...

Keyword(s):

Sertoli Cells ◽

Normal Values ◽

Accessory Gland ◽

Plasma Testosterone ◽

Cell Multiplication ◽

Daily Production ◽

Testicular Growth ◽

Adult Mice ◽

Snell Dwarf ◽

Dwarf Mice

Abstract. Dwarf mice show delayed testicular growth and their adult testis weights are half the normal value. The aims of the present work were firstly, to compare the developmental profiles of plasma gonadotropins and of testicular cell multiplication and differentiation in dwarf vs normal mice and secondly, to determine the effect of hMG supplementation on dwarf mice. In the dwarf mice no pubertal rise in plasma FSH was observed, and the adult values remained very low when compared with those of normal mice; plasma LH decreased after 40 days of age and remained equal to half the normal values. In adults, testicular testosterone content was greatly increased in dwarf mice compared with normal mice, whereas plasma testosterone and accessory gland weights were reduced. At 24 days of age, the total numbers per testis of Leydig and Sertoli cells were reduced in dwarf vs normal mice, whereas in adult mice their differentiation, but not their total numbers, was reduced. This resulted in lower daily production of leptotene primary spermatocytes and of round spermatids in dwarf than in normal mice. hMG supplementation promoted Leydig and Sertoli cell multiplication, but did not produce full differentiation, resulting in increased daily production of round spermatids. In conclusion, in adult dwarf mice a deficiency in plasma gonadotropins prevents full differentiation of Leydig and Sertoli cells without affecting the number of these cells.

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

Journal of Endocrinology ◽

10.1677/joe.0.0920405 ◽

1982 ◽

Vol 92 (3) ◽

pp. 405-407 ◽

Cited By ~ 25

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.

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Further evidence of inactivity of hypothalamo-pituitary-thyroid axis in snell dwarf mice

The Anatomical Record ◽

10.1002/ar.1092100409 ◽

1984 ◽

Vol 210 (4) ◽

pp. 617-627 ◽

Cited By ~ 4

Author(s):

Andrzej Lewi?ski ◽

Andrzej Bartke ◽

Kalman Kovacs ◽

Lyn Richardson ◽

Nancy K. R. Smith

Keyword(s):

Pituitary Thyroid Axis ◽

Snell Dwarf ◽

Thyroid Axis ◽

Dwarf Mice

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Regulation of testicular human chorionic gonadotrophin binding in prolactin-deficient Snell dwarf mice

Journal of Endocrinology ◽

10.1677/joe.0.0950301 ◽

1982 ◽

Vol 95 (3) ◽

pp. 301-309 ◽

Cited By ~ 11

Author(s):

A. G. Amador ◽

A. Bartke

Keyword(s):

Leydig Cells ◽

Chorionic Gonadotrophin ◽

Human Chorionic Gonadotrophin ◽

Direct Effects ◽

Down Regulation ◽

Drug Induced ◽

Congenital Deficiency ◽

Similar Dose ◽

Snell Dwarf ◽

Dwarf Mice

The regulation of binding of 125I-labelled human chorionic gonadotrophin (hCG) to testis was studied in mutant mice with congenital deficiency of prolactin (dw/dw), in mice with prolactin deficiency induced by treatment with bromocriptine and in normal untreated mice. After injection of hCG, normal mice showed a dose-related decrease in testicular hCG binding and subsequent recovery from down-regulation, similar to previous findings in the rat. Mice with congenital prolactin deficiency had a similar dose–response curve of receptor loss after hCG administration, but recovered from down-regulation faster than the normal mice. Induction of prolactin deficiency with bromocriptine prevented down-regulation of hCG binding. The differential effects of congenital and drug-induced prolactin deficiency could be related to a difference in the duration of the deficiency or to its severity. However, this difference could also suggest direct effects of the dw mutation and/or bromocriptine on the Leydig cells.

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

Journal of Endocrinology ◽

10.1677/joe.0.1260193 ◽

1990 ◽

Vol 126 (2) ◽

pp. 193-201 ◽

Cited By ~ 38

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

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

Parasitology ◽

10.1017/s0031182000082974 ◽

1983 ◽

Vol 87 (3) ◽

pp. 447-453 ◽

Cited By ~ 7

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.

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Nrf2 Signaling, a Mechanism for Cellular Stress Resistance in Long-Lived Mice

Molecular and Cellular Biology ◽

10.1128/mcb.01145-09 ◽

2009 ◽

Vol 30 (3) ◽

pp. 871-884 ◽

Cited By ~ 103

Author(s):

Scott F. Leiser ◽

Richard A. Miller

Keyword(s):

Stress Resistance ◽

Uv Light ◽

Antioxidant Response ◽

Membrane Lipid ◽

Mrna Levels ◽

Plasma Membrane Lipid ◽

Snell Dwarf ◽

As Stress ◽

Dwarf Mice

ABSTRACT Transcriptional regulation of the antioxidant response element (ARE) by Nrf2 is important for the cellular adaptive response to toxic insults. New data show that primary skin-derived fibroblasts from the long-lived Snell dwarf mutant mouse, previously shown to be resistant to many toxic stresses, have elevated levels of Nrf2 and of multiple Nrf2-sensitive ARE genes. Dwarf-derived fibroblasts exhibit many of the traits associated with enhanced activity of Nrf2/ARE, including higher levels of glutathione and resistance to plasma membrane lipid peroxidation. Treatment of control cells with arsenite, an inducer of Nrf2 activity, increases their resistance to paraquat, hydrogen peroxide, cadmium, and UV light, rendering these cells as stress resistant as untreated cells from dwarf mice. Furthermore, mRNA levels for some Nrf2-sensitive genes are elevated in at least some tissues of Snell dwarf mice, suggesting that the phenotypes observed in culture may be mirrored in vivo. Augmented activity of Nrf2 and ARE-responsive genes may coordinate many of the stress resistance traits seen in cells from these long-lived mutant mice.

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