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Abstract
11 β-Hydroxysteroid dehydrogenase (11β-HSD) catalyses the reversible metabolism of corticosterone to inert 11-dehydrocorticosterone. At least two isoforms exist. 11β-HSD-1, the first to be characterised and the only isoform for which a cDNA has been isolated, is highly expressed in liver, kidney and hippocampus. The activity of 11β-HSD in rat liver is higher in males, due to oestrogen repression of 11β-HSD-1 gene transcription in females. Sexual dimorphism in rodent liver proteins is frequently mediated indirectly via sex-specific patterns of GH release (continuous in females, pulsatile in males). We have now investigated whether this applies to 11β-HSD, using dwarf rats (congenitally deficient in GH) and hypophysectomised animals.
11β-HSD activity and 11β-HSD-1 mRNA expression in liver was significantly lower in control female than male rats (50% and 72% of male levels respectively). These sex differences in the liver were attenuated in dwarf rats, with both males and females showing similar levels of 11 β-HSD activity to control males. Administration of continuous (female pattern) GH to dwarf male rats decreased hepatic 11β-HSD activity (30% fall) and mRNA expression (77% fall), whereas the same total daily dose of GH given in the male (pulsatile) pattern had no effect on hepatic 11 β-HSD in female dwarf rats. Continuous GH also attenuated hepatic 11 β-HSD activity (25% fall) and 11β-HSD-1 mRNA expression (82% fall) in hypophysectomised animals. However, oestradiol itself suppressed hepatic 11β-HSD activity (25% fall) and 11β-HSD-1 mRNA expression (60% fall) in hypophysectomised rats.
Renal 11 β-HSD activity showed no sexual dimorphism in control or dwarf rats, although overall activity was lower in dwarf animals. By contrast, 11β-HSD-1 mRNA expression was higher in male than female kidney in both control and dwarf strains. Neither GH pattern had any effect on 11β-HSD activity or 11β-HSD-1 mRNA levels in the kidney of dwarf rats, although continuous GH attenuated 11β-HSD activity (28% fall) and 11β-HSD-1 mRNA expression in kidney (47% decrease) in hypophysectomised animals. Oestradiol attenuated renal 11β-HSD-1 mRNA expression (74% fall) in hypophysectomised rats, but increased enzyme activity (62% rise) in the kidney. None of the manipulations had any effect on hippocampal 11 β-HSD activity or gene expression.
These data demonstrate the following. (i) Sexual dimorphism of hepatic 11β-HSD is mediated, in part, via sex-specific patterns of GH secretion acting on 11β-HSD-1 gene expression. (ii) There is an additional direct repressive effect of oestrogen on hepatic 11β-HSD-1. (iii) Other tissue-specific factors are involved in regulating 11β-HSD-1, as neither peripheral GH nor oestrogen have effects upon hippocampal 11β-HSD-1. (iv) The regulation of 11β-HSD-1 mRNA expression in the kidney broadly parallels the liver. The lack of correlation between changes in expression of the 11β-HSD-1 gene and renal 11β-HSD activity reflects the presence of an additional gene product(s) in the kidney, the expression of which is largely independent of GH.
Journal of Endocrinology (1994) 143, 541–548
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). Discussion We observed sexual dimorphism in insulin sensitivity, function and morphology of prepubertal, pubertal, and adult rat pancreatic islets, and susceptibility to develop diabetes. To our knowledge, this is the first report showing that serum
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School of Molecular Biosciences, Veterinary Microbiology and Pathology, Animal Sciences, Departments of
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shown). Lean fat-free mass was greater in both sexes of Mstn −/− mice and total and percent body fat content was less ( Fig. 1 A), particularly in females. This sexual dimorphism in adiposity among Mstn −/− mice is highly novel and to our knowledge
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ABSTRACT
Inhibin was partially purified from bovine follicular fluid using chromatography on immobilized Procion Red 3B and anion-exchange chromatography. Ovariectomized Texel ewes were immunized against the inhibin-containing fraction from the Procion Red 3B column and the immune response was subsequently boosted with similar fractions or with the preparation obtained from the anion-exchange column. The potencies of the resulting antisera were evaluated in an invitro bioassay system for estimating inhibin activity, using dispersed rat pituitary cells. The antisera were found to inhibit the bioactivity of inhibin preparations from ovarian follicular fluid of bovine, porcine, ovine or human origin, as well as inhibin activity in ovine testicular lymph and rete testis fluid, in culture media from rat granulosa and rat Sertoli cells and in homogenates of rat ovaries and testes. These results indicate that the inhibin molecules from several species contain a common bioactive moiety. The results also showed that the antiserum was more effective in neutralizing inhibin activity from ovarian than from testicular sources in both sheep and rat, indicating a sex-related difference in the inhibin molecules within a species.
J. Endocr. (1986) 111, 255–261
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ABSTRACT
Temporal plasma GH secretory patterns were measured in cannulated male and female meat-type chickens of two commercial strains at 17, 38 and 60 days of age. Pulse height, amplitude and baseline values were similar in both male and female chickens at 17 days of age, with high amplitude and low baseline values. However, by 38 days of age pulsatile GH secretion was not detectable in females, whereas males exhibited a continued pulsatile secretory pattern similar to that at 17 days of age. Pulsatile GH secretion was not evident in either males or females at 60 days of age. These results clearly demonstrate a sexually dimorphic ontogeny of GH secretion in meat-type chickens.
J. Endocr. (1988) 119, 101–109
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Synapses develop at similar rates in the suprachiasmatic nucleus of rats of both sexes, but values are higher in male than in female animals from birth to maturity. Male-type development cannot be mimicked by neonatal androgenization but results suggest that female-type development can be induced by neonatal castration of males. The results suggested that both prenatal and postnatal androgens are essential to normal male development.
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SUMMARY
Adult male rats were treated with daily s.c. doses of 10 mg. cyproterone acetate for 3 weeks. Histological examination of the exorbital lacrimal glands at the end of treatment showed distinct differences compared with male controls: the histological picture showing greater resemblance to the glands of female controls. In orchidectomized rats receiving substitution treatment with testosterone propionate, cyproterone acetate 'neutralized' the effect of testosterone propionate on the exorbital lacrimal gland to a considerable extent. The possibility that this gland may play a part in the sexual behaviour of the rat is discussed.
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ABSTRACT
The post-hatch ontogeny of hepatic GH binding and its relationship to GH plasma profile characteristics in male and female turkeys of slow- (RBC-2) and fast-growing (F; selected from RBC-2) genetic lines were determined. Specific binding of 125I-labelled recombinant chicken GH to crude hepatic membrane preparations (100 000 g pellet) was determined at 2, 4, 8, 14 and 24 weeks of age for both total (occupied plus free; 4 mol MgCl2/l pretreatment) and free (without MgCl2 pretreatment) binding sites. Characteristics of the plasma GH profile were measured at each age by serial blood sampling through indwelling jugular vein catheters.
When specific binding to either free or total sites was expressed on a whole organ basis (i.e. hepatic GH-binding capacity/bird), binding increased dramatically (P < 0·0001) with increasing age over both lines and sexes. Total binding capacity (free plus occupied sites) per bird was greater for females than for males at 24 weeks of age (P < 0·04), as birds reached sexual maturity, but did not differ between fast- and slow-growing lines at any age. Available binding capacity (free sites) per bird was greater for the faster growing F than RBC-2 line at the older ages when body size was most divergent (14 and 24 weeks of age; P < 0·01, P < 0·06 respectively), but did not differ between sexes.
Correlation analysis at individual ages revealed a progressive change in the nature of the relationship between hepatic GH binding, plasma GH and somatic growth. At 2 weeks of age, when growth velocity of these birds was high relative to later ages, there were no significant correlations among hepatic GH binding, plasma GH and somatic growth. Thereafter, the correlation between total binding capacity and plasma GH concentration progressed from positive (r = 0·34; P < 0·16) to no correlation (r = −0·01; P< 0·97) to increasingly negative, until at the oldest age studied (24 weeks), the correlation was strongly negative (r = −0·55) and significant (P < 0·03). At the older ages, hepatic binding became significantly correlated to measures of somatic growth.
These results indicate that no consistent relationship exists between hepatic GH binding and plasma GH status, over all ages, lines and sexes. Rather different relationships exist at different ages/physiological states. In the growth-divergent lines of turkeys studied here, measures of somatic growth are most strongly correlated with hepatic GH binding at later ages, after the early period of most rapid growth is past, and as mature body size and onset of sexual maturity are approached. The phenomenon of down-regulation of hepatic GH binding as birds approach sexual maturity was suggested by a significant negative correlation between total binding sites and plasma GH at that time.
Journal of Endocrinology (1990) 126, 131–139
Paul Langerhans Institute Dresden (PLID), Helmholtz Center Munich, University Hospital and Faculty of Medicine, TU Dresden, Dresden, Germany
German Center for Diabetes Research (DZD e.V.), Neuherberg, Germany
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Paul Langerhans Institute Dresden (PLID), Helmholtz Center Munich, University Hospital and Faculty of Medicine, TU Dresden, Dresden, Germany
German Center for Diabetes Research (DZD e.V.), Neuherberg, Germany
Diabetes and Nutritional Sciences, King's College London, London, UK
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Paul Langerhans Institute Dresden (PLID), Helmholtz Center Munich, University Hospital and Faculty of Medicine, TU Dresden, Dresden, Germany
German Center for Diabetes Research (DZD e.V.), Neuherberg, Germany
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factors that have also been also associated with sexual-gender dimorphism in insulin resistance ( Sarlio-Lahteenkorva & Lahelma 1999 , Dallongeville et al. 2005 , Hwang & Lee 2014 , Xu et al. 2016 ). Finally, we are going to discuss open research
