propose that ROS could be involved in the sexual dimorphism found in thyroid dysfunctions. Future studies are necessary to evaluate the involvement of NOX4-generated ROS in the estrogen-signaling pathway in thyrocytes. Elucidating this issue is crucial to
Rodrigo S Fortunato, Andrea C F Ferreira, Fabio Hecht, Corinne Dupuy and Denise P Carvalho
Filip Callewaert, Mieke Sinnesael, Evelien Gielen, Steven Boonen and Dirk Vanderschueren
the pathophysiology of osteoporosis and osteoporotic fracture risk in men. Skeletal gender differences in radial bone growth (skeletal sexual dimorphism) are traditionally attributed to stimulatory ‘male’ androgen action as opposed to inhibitory
I. M. Adcock and B. D. Greenstein
The rat brain is sexually dimorphic with respect to structure and function, and there is evidence that these differences are effected in the fetus through changes in protein synthesis, some of which may result from the intervention of gonadal steroids. To investigate this, messenger RNA (mRNA) from the limbic system and cerebellum of neonatal rats was prepared, translated in a rabbit reticulocyte system in vitro and the products were analysed by two-dimensional electrophoresis and fluorography. Some of the results were further analysed using image analysis. There was a striking sexual dimorphism in the patterns of incorporation of [35S]methionine into proteins using mRNA from the limbic system, in that groups of proteins were apparently present in male-but not in female-derived fluorograms and vice versa. One protein, tentatively identified from its coordinates as α-tubulin, was more abundant in male-derived fluorograms. Although there were no clear-cut qualitative sex differences using mRNA derived from the cerebellum, that derived from the male cerebellum appeared to be consistently more active. These results provide direct evidence for a sexual dimorphism at the transcriptional level in the neonatal limbic system of the rat.
J. Endocr. (1986) 109, 23–28
Y Fukazawa, T Iguchi and H A Bern
The anococcygeus muscle (AcM) is one of a pair of thin sheets of smooth muscle inserting on the rectum, having a tendinous origin largely on sacral vertebrae. The cross-sectional area of AcM in the juxtarectal region in 90-day-old male mice was significantly larger than that in females of three strains: BALB/cCrgl, ICR/Jcl and C57BL/Tw. The AcM area in female mice showed strain differences: BALB/c>ICR>C57BL. Five daily injections of testosterone into newborn ICR mice from the day of birth significantly increased the areas of AcM in both sexes at 30 days of age, but five daily injections of oestradiol-17β (OE) decreased them. The AcM area in 60-day-old ICR male mice castrated at 30 days of age was significantly smaller than in intact males, and that in ovariectomized females was significantly larger than in intact females. In both sexes, implantation of a testosterone pellet (12 mg) into gonadectomized mice on the day of gonadectomy stimulated the growth of AcM, and implantation of an OE pellet (12 mg) inhibited the growth of AcM. The AcM in both ICR and C57BL strains showed positive androgen receptor and oestrogen receptor immunostaining at 15 days. Female ICR mice exposed neonatally to diethylstilboestrol (DES) had significantly larger AcM than controls; ovariectomy at 30 days of age did not change the AcM area in 60-day-old DES-exposed mice. However, male mice exposed neonatally to DES had significantly smaller AcM than controls; castration at 30 days of age nullified this inhibition. These results suggest that both androgen and oestrogen play an important role in sexual dimorphism of the mouse AcM. Neonatal exposure to DES (but not to oestradiol) had an irreversible stimulatory effect on the AcM area in female mice.
Journal of Endocrinology (1997) 152, 229–237
A. EL HANI, M. DALLE and P. DELOST
Sexual dimorphism in adrenal activity appeared during the pubertal period of the guinea-pig with plasma levels and binding of cortisol lower in male guinea-pigs compared with female, and metabolic clearance rate (MCR) of cortisol higher in male than in female animals. Gonadectomy of female guinea-pigs did not change the values of the parameters regulating adrenal activity. Castration of male guinea-pigs caused a rise in plasma cortisol levels by increasing the binding capacity of transcortin for cortisol and by decreasing cortisol MCR. Treatment of females with testosterone from day 24 produced a drop on day 50 in plasma cortisol levels following a decreased binding capacity of transcortin for cortisol and at the same time as cortisol MCR increased. Furthermore, the adrenal response to stress was higher in castrated than in control males and lower in testosterone-treated females compared with control females. Testosterone appeared to be the hormone responsible for sexual dimorphism in adrenal activity in the pubertal guinea-pig.
W. D. Booth
Submaxillary glands of mature Göttingen miniature pigs were examined for the presence of a sexual dimorphism. Gland weights, serous cell hypertrophy and total protein in the glands were much greater in male than female pigs. High concentrations of the pheromonal 16-androstene steroids were present in the glands of males and exceeded 2 mmol/g in some animals; this was primarily due to 5α-androst-16-en-3α-ol. The high concentration of 16-androstene steroids in boar glands was correlated with the presence of large amounts of binding protein for these steroids in the glands; smaller amounts of the binding protein were detected in female glands. These findings are similar to those found in domestic pigs, but the degree of sexual dimorphism assessed from these findings is more extreme in the miniature pig.
J. Endocr. (1984) 100, 195-202
Andrés J López-Contreras, Jesús D Galindo, Carlos López-García, Maria T Castells, Asunción Cremades and Rafael Peñafiel
. 1973 , Middleton et al . 1987 , Middleton & Bulfield 1988 ). In contrast, little is known about the influence of sex hormones on the regulation of DDC in murine tissues. The possible existence of sexual dimorphism in catecholamine metabolism could be
Paz Vital, Elena Larrieta and Marcia Hiriart
). 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
Melissa F Jackson, Dung Luong, Dor Dor Vang, Dilip K Garikipati, James B Stanton, O Lynne Nelson and Buel D Rodgers
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
S C Low, K E Chapman, C R W Edwards, T Wells, I C A F Robinson and J R Seckl
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