Effects of castration and sex steroid treatment on the motor copulatory pattern of the rat

1981 ◽  
Vol 27 (4) ◽  
pp. 727-730 ◽  
Author(s):  
C. Beyer ◽  
J.L. Contreras ◽  
G. Moralí ◽  
K. Larsson
Keyword(s):  
Steroid Treatment ◽  
Sex Steroid ◽  
Copulatory Pattern

scholarly journals Differential Expression of Na+/H+-Exchanger (NHE-1, 2, and 4) Proteins and mRNA in Rodent’s Uterus under Sex Steroid Effect and at Different Phases of the Oestrous Cycle

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Khadijeh Gholami ◽  
Sekaran Muniandy ◽  
Naguib Salleh
Keyword(s):  
Real Time Pcr ◽  
Apical Membrane ◽  
Ph Regulation ◽  
Steroid Treatment ◽  
Oestrous Cycle ◽  
Sex Steroid ◽  
Vaginal Smear ◽  
Uterine Fluid ◽  
Mrna And Protein Expression ◽  
Nhe Isoforms

Precise uterine fluid pH regulation may involve the Na+/H+-exchanger (NHE). We hypothesized that NHE isoforms are differentially expressed under different sex steroid treatment and at different oestrous cycle phases which may explain the uterine fluid pH changes observed under these conditions.Method. Oestrous cycle phases of intact WKY rats were identified by vaginal smear. Another group of rats was ovariectomized and treated with 0.2 μg 17β-oestradiol (E), 4 mg progesterone (P), and E followed by P (E + P). The animals were then sacrificed and the uteri were removed for mRNA and protein expression analyses by real-time PCR and western blotting, respectively. NHE isoforms distribution was detected by immunohistochemistry (IHC).Results. NHE-1 mRNA and protein were upregulated at diestrus (Ds) and following P treatment. Meanwhile, NHE-2 and NHE-4 proteins and mRNA were upregulated at proestrus (Ps) and estrus (Es) and following E treatment. NHE-1 was found predominantly at the apical membrane, while NHE-2 and NHE-4 were found at the apical and basolateral membranes of the luminal epithelia. NHE-4 is the main isoform upregulated by E.Conclusion. Differential expressions of uterine NHE isoforms 1, 2, and 4 could explain the observed changes in the uterine fluid pH under these conditions.

scholarly journals Sex Steroid Treatment of Constitutionally Tall Stature*

1998 ◽  
Vol 19 (5) ◽  
pp. 540-558 ◽  
Author(s):  
Stenvert L. S. Drop ◽  
Wouter J. de Waal ◽  
Sabine M. P. F. de Muinck Keizer-Schrama
Keyword(s):  
Steroid Treatment ◽  
Sex Steroid ◽  
Tall Stature

scholarly journals Long term sequelae of sex steroid treatment in the management of constitutionally tall stature.

1995 ◽  
Vol 73 (4) ◽  
pp. 311-315 ◽  
Author(s):  
W J de Waal ◽  
M Torn ◽  
S M de Muinck Keizer-Schrama ◽  
R S Aarsen ◽  
S L Drop
Keyword(s):  
Steroid Treatment ◽  
Sex Steroid ◽  
Tall Stature

scholarly journals Effects of the Timing of Sex-Steroid Exposure in Adolescence on Adult Health Outcomes

2019 ◽  
Vol 104 (10) ◽  
pp. 4578-4586 ◽  
Author(s):  
Yee-Ming Chan ◽  
Amalia Feld ◽  
Elfa Jonsdottir-Lewis
Keyword(s):  
Turner Syndrome ◽  
Klinefelter Syndrome ◽  
Pubertal Timing ◽  
Steroid Treatment ◽  
Endocrine Function ◽  
Mr Studies ◽  
Sex Steroid ◽  
Adult Health ◽  
Wide Range ◽  
Constitutional Delay

Abstract Context Variation in pubertal timing is associated with a wide range of adult risks and outcomes, but it is unclear whether these associations are causal, and it is largely unknown whether these associations can be modified by treatment. Evidence Acquisition We conducted PubMed searches to identify Mendelian randomization (MR) studies on the influence of pubertal timing on adult health and studies on sex-steroid treatment of the following conditions associated with reduced reproductive endocrine function in adolescence: constitutional delay, Turner syndrome, and Klinefelter syndrome. Evidence Synthesis Results of MR studies suggest that earlier pubertal timing increases body mass index; increases risk for breast, ovarian, endometrial, and prostate cancers; elevates fasting glucose levels and blood pressure; impairs lung capacity and increases risk for asthma; leads to earlier sexual intercourse and first birth; decreases time spent in education; and increases depressive symptoms in adolescence. Later pubertal timing appears to lower bone mineral density (BMD). Although studies of constitutional delay have not shown that sex-steroid treatment alters adult height or BMD, studies of girls with Turner syndrome and boys with Klinefelter syndrome suggest that earlier initiation of sex-steroid treatment improves physical and neurocognitive outcomes. Conclusions Despite having some limitations, MR studies suggest that pubertal timing causally influences many adult conditions and disease risks. Studies of Turner syndrome and Klinefelter syndrome suggest that earlier sex-steroid exposure may have short- and long-term benefits. The mechanisms underlying these findings and the effects of trends and treatments affecting pubertal timing remain to be determined.

scholarly journals Complex regulation of GH autofeedback under dual-peptide drive: studies under a pharmacological GH and sex steroid clamp

2011 ◽  
Vol 300 (6) ◽  
pp. E1158-E1165 ◽  
Author(s):  
Johannes D. Veldhuis ◽  
Dana Erickson ◽  
John M. Miles ◽  
Cyril Y. Bowers
Keyword(s):  
Sex Difference ◽  
Negative Feedback ◽  
Approximate Entropy ◽  
Hormone Treatment ◽  
Steroid Treatment ◽  
Saline Infusion ◽  
Sex Steroid ◽  
Double Blind ◽  
Gh Secretion ◽  
Peptide Stimulation

To test the postulate that sex difference, sex steroids, and peptidyl secretagogues control GH autofeedback, 11 healthy postmenopausal women and 14 older men were each given 1) a single iv pulse of GH to enforce negative feedback and 2) continuous iv infusion of saline vs. combined GHRH/GHRP-2 to drive feedback escape during pharmacological estradiol (E2; women) or testosterone (T; men) supplementation vs. placebo in a double-blind, prospectively randomized crossover design. By three-way ANCOVA, sex difference, sex hormone treatment, peptide stimulation, and placebo/saline responses (covariate) controlled total (integrated) GH recovery during feedback (each P < 0.001). Both sex steroid milieu ( P = 0.019) and dual-peptide stimulation ( P < 0.001) determined nadir (maximally feedback-suppressed) GH concentrations. E2/T exposure elevated nadir GH concentrations during saline infusion ( P = 0.003), whereas dual-peptide infusion did so independently of T/E2 and sex difference ( P = 0.001). All three of sex difference ( P = 0.001), sex steroid treatment ( P = 0.005), and double-peptide stimulation ( P < 0.001) augmented recovery of peak (maximally feedback-escaped) GH concentrations. Peak GH responses to dual-peptidyl agonists were greater in women than in men ( P = 0.016). E2/T augmented peak GH recovery during saline infusion ( P < 0.001). Approximate entropy analysis corroborated independent effects of sex steroid treatment ( P = 0.012) and peptide infusion ( P < 0.001) on GH regularity. In summary, sex difference, sex steroid supplementation, and combined peptide drive influence nadir, peak, and entropic measurements of GH release under controlled negative feedback. To the degree that the pharmacological sex steroid, GH, and dual-peptide clamps provide prephysiological regulatory insights, these outcomes suggest major determinants of pulsatile GH secretion in the feedback domain.

Reduced free IGF-I and increased IGFBP-3 proteolysis in Turner syndrome: modulation by female sex steroids

2001 ◽  
Vol 280 (2) ◽  
pp. E308-E314 ◽  
Author(s):  
Claus Højbjerg Gravholt ◽  
Jan Frystyk ◽  
Allan Flyvbjerg ◽  
Hans Ørskov ◽  
Jens Sandahl Christiansen
Keyword(s):  
Turner Syndrome ◽  
Final Height ◽  
Steroid Treatment ◽  
Sex Steroid ◽  
Female Sex ◽  
Igf I ◽  
Igf Binding ◽  
17Β Estradiol ◽  
Igf Binding Protein ◽  
Igfbp 3

The bioactivity of the growth hormone-insulin-like growth factor (IGF) system is reduced in Turner syndrome and may explain the reduction seen in final height. We compared levels of free and total IGF-I, immunoreactive and Western ligand blot IGF-binding protein (IGFBP)-3, and IGFBP-3 proteolysis in women with Turner syndrome ( n = 23) before (TB) and during 6 mo treatment with 17β-estradiol and norethisterone. An age-matched group of controls ( n = 24) was included. Total IGF-I and immunoreactive levels of IGFBP-3 were comparable in TB and controls, whereas free IGF-I ( P = 0.02) in TB was less than in controls. Western ligand blotting (WLB)-IGFBP-3 was significantly lower in TB than in controls ( P = 0.0005). Accordingly, IGFBP-3 proteolysis was greater in Turner syndrome ( P = 0.001). Female sex steroid treatment increased WLB-IGFBP-3 ( P = 0.0005), whereas immunoreactive IGFBP-3 and IGFBP-3 proteolysis were normalized ( P = 0.004). Free IGF-I remained unchanged ( P = 0.8), with a tendency toward a decrease in total IGF-I ( P = 0.1). In conclusion, despite normal total IGF-I and immunoreactive IGFBP-3, free serum IGF-I is less and IGFBP-3 proteolysis is greater in Turner syndrome than in controls. During sex steroid treatment, IGFBP-3 proteolysis normalized, without any change in free IGF-I.

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