Search Results
Search for other papers by S. Jeffery in
Google Scholar
PubMed
Search for other papers by C. A. Wilson in
Google Scholar
PubMed
Search for other papers by A. Mode in
Google Scholar
PubMed
Search for other papers by J.-Å. Gustafsson in
Google Scholar
PubMed
Search for other papers by N. D. Carter in
Google Scholar
PubMed
ABSTRACT
Rat liver exhibits a reversed sexual dimorphism of its two endogenous soluble carbonic anhydrase (CA) isozymes, CA II and CA III. Normal males have hepatic CA III concentrations ten–twenty times those in the female, while female liver contains two–three times more CA II than the male. Hypophysectomy abolishes this sexual differentiation, having no effect on male liver but producing isozyme concentrations in the female liver similar to those in the male. Infusion of a continuous level of GH into male rats induces a female-like isozyme pattern for both CA II and CA III.
J. Endocr. (1986) 110, 123–126
Search for other papers by C Rivier in
Google Scholar
PubMed
Abstract
The bilateral communication between the immune and neuroendocrine systems plays an essential role in modulating the adequate response of the hypothalamic-pituitary-adrenal (HPA) axis to the stimulatory influence of interleukins (ILs). It is thus reasonable to assume that inappropriate responses of the HPA axis to ILs might play a role in modulating the onset of pathological conditions such as infections. As part of our programme aimed at investigating the ability of ILs to release pro-opiomelanocortin-like peptides and corticosterone in rats exposed to alcohol, we observed that this stimulatory action appeared to be influenced by the gender of the animals. We therefore examined the ability of IL-1β, injected peripherally, to stimulate the HPA axis as a function of stage of sexual maturation and the presence or absence of circulating sex steroids.
In immature (21 to 22-day-old) rats, both males and females responded to the i.p. administration of 0·5 or 2·0 μg IL-1β/kg with statistically comparable increases in plasma ACTH levels. In contrast, females released significantly (P<0·01) more corticosterone in response to the lower dose of cytokine. Forty-day-old intact animals showed no sexual dimorphism in ACTH secretion, but the females again secreted significantly (P<0·05–0·01) more corticosterone. Gonadectomy, performed 7–8 days prior to the assay, increased the absolute amount of corticosterone released over a 60-min period. A noticeable dimorphism of the ACTH response to IL-1β became apparent in 70-day-old intact rats, with females secreting more ACTH than males. These females also released significantly more corticosterone than males under both resting and stimulated circumstances. In this age group, gonadectomy abolished the sex difference in terms of ACTH release, but augmented the total amount of corticosteroids secreted by both sexes, as well as increasing the sexual dimorphism.
These results suggest the presence of gender differences in the response of the HPA axis to IL-1β. While the sexual dimorphism of ACTH secretion appears to be dependent on circulating sex steroids, the sexually dimorphic adrenal response was retained following gonadectomy.
Journal of Endocrinology (1994) 140, 365–372
Search for other papers by H. F. URBANSKI in
Google Scholar
PubMed
Search for other papers by B. K. FOLLETT in
Google Scholar
PubMed
Plasma levels of LH are generally higher in male than in female quail. This dimorphism was found to persist in quail which had been through a breeding cycle and then gonadectomized. Under long daylengths (12 h light: 12 h darkness (12L : 12D) or 16L : 8D) ovariectomized quail had plasma levels of LH that were 55–70% of those seen in castrated birds. The difference was reduced after transfer to short days (8L : 16D) when LH concentrations fell to basal levels, but again became more pronounced when the quail were restimulated with long photoperiods. Thus, the photoperiodic response system is sexually differentiated.
Search for other papers by B. D. Greenstein in
Google Scholar
PubMed
Search for other papers by I. M. Adcock in
Google Scholar
PubMed
ABSTRACT
There is sexual dimorphism of specific species of mRNA in the neonatal rat brain and this sexual dimorphism may be imprinted by steroids of testicular origin during the perinatal period. According to current theories, only aromatizable androgens may cause sexual differentiation of sexual behaviour and function in the adult. The effects of oestradiol benzoate on mRNA synthesis in the neonatal female limbic system were therefore studied. In addition, cytosolic and nuclear oestrogen receptors were measured after administration of testosterone propionate, oestradiol benzoate or dihydrotestosterone (DHT). An attempt was made to distinguish between the brain oestrogen receptor and the plasma oestrogen-binding protein, alphafoetoprotein (AFP) by isoelectric focussing. After injection of 50 μg oestradiol benzoate s.c. to neonatal female rats, the expression of mRNA coding for sexually dimorphic proteins appeared to be changed to a male-type pattern. The overall density of labelling was noticeably greater and specific changes in labelled proteins were observed. These effects were observed within 3 h of injection. Both testosterone and oestradiol caused a marked depletion of cytosolic oestrogen receptors in the limbic system whereas DHT was ineffective in this respect. Nuclear receptors were present in equal abundance in male- and female-derived nuclei and only oestradiol was able to cause a significant (P < 0·025) increase in nuclear oestrogen receptors. The receptor and AFP could be distinguished by isoelectric focussing, since the pI of the receptor was 7·05, while that of AFP was 4·5. These results are consistent with the possibility that oestradiol alters transcription in the neonatal rat brain and may do this through the oestrogen receptor. Nevertheless, it is also possible that oestradiol could alter post-transcriptional events such as the stability of mRNA or the binding of tRNA to the polysomal complex.
Journal of Endocrinology (1989) 120, 83–88
Search for other papers by Ch. Jean-Faucher in
Google Scholar
PubMed
Search for other papers by M. Berger in
Google Scholar
PubMed
Search for other papers by Ch. Gallon in
Google Scholar
PubMed
Search for other papers by M. de Turckheim in
Google Scholar
PubMed
Search for other papers by G. Veyssière in
Google Scholar
PubMed
Search for other papers by Cl. Jean in
Google Scholar
PubMed
ABSTRACT
Kidneys of adult male mice are larger than those of females because of both cellular hyperplasia and hypertrophy. Administration of testosterone to adult female mice induced cellular hypertrophy but not hyperplasia, so that the weight of the kidney remained smaller than in male mice. The sexual dimorphism in kidney size is not congenital but programmed by neonatal endogenous androgens and expressed between 30 and 40 days of age. Treatment of newborn males with cyproterone acetate and of newborn females with testosterone induced female and male patterns of renal growth respectively. It appears that neonatal endogenous androgens are required to induce the characteristic cellular hyperplasia of the kidneys of male mice. Manipulation of androgen levels during neonatal and prepubertal life was found to affect the growth response of the kidney to androgens in adult male and female mice.
J. Endocr. (1987) 115, 241–246
Search for other papers by M. Nonomura in
Google Scholar
PubMed
Search for other papers by K. Hoshino in
Google Scholar
PubMed
Search for other papers by T. Harigaya in
Google Scholar
PubMed
Search for other papers by H. Hashimoto in
Google Scholar
PubMed
Search for other papers by O. Yoshida in
Google Scholar
PubMed
ABSTRACT
Hyperprolactinaemia induced by pituitary isografts in male host mice was confirmed by radioimmunoassay, but plasma testosterone levels determined by radioimmunoassay in these mice showed no changes. Immunoenzyme electron microscopic observations revealed large spherical-shaped immunoreactive prolactin granules in pituitary grafts in male hosts, regardless of the sex of the donor mice, indicating the disappearance of sexual dimorphism in prolactin-producing cells in hyperprolactinaemic mice. In hyperprolactinaemic host mice the male accessory sex glands, particularly the seminal vesicle and the ventral prostate, exhibited considerable proliferation and significant increase in weight. These phenomena do not seem to be mediated by the increased action of testosterone. Such biological effects in host mice were much greater when the donor was female rather than male, and were more noticeable in C57BL mice than in C3H mice.
J. Endocr. (1985) 107, 71–76
Search for other papers by W. D. BOOTH in
Google Scholar
PubMed
SUMMARY
Testosterone and 5α-dihydrotestosterone were extracted from the submaxillary salivary glands of boars at different ages, but were not detected in these glands of the female pig. After purification by thin-layer and paper chromatography the steroids were identified by gas—liquid chromatography and combined gas—liquid chromatography—mass spectrometry. In the submaxillary gland of the mature boar, a high concentration of androgen (> l μg/100 g) was found, and the concentration of 5α-dihydrotestosterone was two to four times higher than testosterone. Immediate steroid precursors of testosterone which are found in boar testis were not isolated. The isolation of the two potent androgens, and the known occurrence of 16-unsaturated C19 steroids in the boar submaxillary gland, shows that there is a biochemical sexual dimorphism in this gland of the pig, which is primarily under the influence of testicular hormones.
Search for other papers by E Ogawa in
Google Scholar
PubMed
Search for other papers by BH Breier in
Google Scholar
PubMed
Search for other papers by I Fujiwara in
Google Scholar
PubMed
Search for other papers by K Iinuma in
Google Scholar
PubMed
Sexual dimorphism of somatic growth in rats appears to reflect differing actions of sex steroids. However, mechanisms of gonadal steroid effects on the somatotropic axis are incompletely understood. To evaluate whether GH is involved in the effects of long-term gonadal suppression on somatic growth in rats, a GnRH agonistic analogue (GnRHa) was administered to normal Sprague-Dawley rats (controls) and to a strain of rats with complete growth hormone deficiency (GHD; n=4-6 in each group). Subcutaneous injection of GnRHa (2 mg/kg) or saline were given within 48 h after birth and repeated every 3 weeks. GnRHa treatment significantly reduced serum gonadal steroid levels in rats of both sexes with small testes in males and impaired development of internal genitalia in females. GnRHa-treated control females became significantly heavier (P<0.01 ANOVA for repeated measures) than saline-treated rats beginning at 8 weeks. However, female GHD rats with GnRHa treatment did not differ in body weight from rats receiving saline. In male rats, GnRHa treatment did not change body weight in either control or GHD rats. Serum IGF-I concentrations did not differ between treatment groups in GHD and control rats of either sex. Hepatic GH binding was reduced significantly by GnRHa treatment in female control rats (P<0.01), but not in female GHD rats. These data suggest that sexual dimorphism in body size and its modulation by estrogens are independent of circulating IGF-I levels suggesting non-endocrine IGF-I-mediated mechanisms, and that GH-induced somatic growth is modulated by estrogens, but not androgens, in rats.
Search for other papers by F. J. C. M. Van Eerdenburg in
Google Scholar
PubMed
Search for other papers by C. M. J. E. Lugard-Kok in
Google Scholar
PubMed
Search for other papers by D. F. Swaab in
Google Scholar
PubMed
ABSTRACT
Postnatal development of the supraoptic nucleus (SON) in the pig hypothalamus was studied morphometrically. The volume of the SON increased from 6·2±0·45 (s.e.m.) mm3 at 7 weeks postnatally to 18·5 ± 1·35 mm3 at 2·5 years of age. A sex difference was found at the development point when the SON volume increased, with earlier SON enlargement in males. This sex difference was 30% at 30 weeks and 50% at 1 year of age. At 2·5 years of age no difference in volume was apparent between the sexes. The number of SON neurones was similar for all age groups concerned (43 500 ± 1475), except for the 2·5year-old females where 40% more were found (55 500 ± 3285). No significant difference was found in neurone number between gonadectomized and sham-operated animals, but the operation caused a 30% reduction in the number of neurones and SON volume. Testosterone supplementation following gonadectomy, during the first 4 weeks postnatally, resulted in sexual dimorphism, the males having more SON neurones than the females. The volume showed only a trend in the same direction. Testosterone supplementation at other ages did not result in any difference when compared with controls.
The results of this study show that the postnatal development of the SON of the pig is sexually dimorphic, and that it continues after puberty in females. In contrast to the vasopressin- and oxytocincontaining nucleus, the development of the SON was not influenced by gonadectomy and only slightly by gonadal steroids.
Journal of Endocrinology (1992) 134, 19–25
Search for other papers by D. A. Carter in
Google Scholar
PubMed
Search for other papers by T. D. M. Williams in
Google Scholar
PubMed
Search for other papers by S. L. Lightman in
Google Scholar
PubMed
ABSTRACT
The influence of endogenous opioids on the posterior pituitary response to stress was investigated by measuring plasma hormone levels in immobilized male and female rats following either acute naloxone treatment or prolonged morphine administration. Naloxone significantly potentiated the oxytocin and arginine vasopressin (AVP) response to immobilization, but in female rats only. The responses of morphine-treated male rats showed differences compared with vehicle-treated controls, although chronic morphine treatment did not reliably alter the oxytocin or AVP responses to immobilization in males or females.
In a further experiment to investigate the role of gonadal hormones in determining the sex difference in responsiveness to naloxone, it was found that acute naloxone treatment significantly potentiated the posterior pituitary response to stress in castrated male rats.
These results extend previous studies showing a sex difference in stress-induced secretion of posterior pituitary hormones, providing evidence of a sexual dimorphism in the endogenous opioid regulation of this response which is partly determined by circulating gonadal hormones.
J. Endocr. (1986) 111, 239–244
