scholarly journals CYP17 gene plays a key role in goose genital growth by influencing the testosterone level at puberty

2018 ◽  
Vol 97 (5) ◽  
pp. 1748-1756 ◽  
Author(s):  
W. Sun ◽  
X. Gan ◽  
J. Hu ◽  
L. Li ◽  
J. Wang
Author(s):  
Sandra Mrozinska ◽  
Tomasz Milewicz ◽  
Iwona Rogatko ◽  
Marta Kialka ◽  
Magdalena Spalkowska ◽  
...  

Author(s):  
Ni Gusti Ayu Manik Ermayanti ◽  
I Gusti Lanang Oka ◽  
I Gede Mahardika ◽  
I Putu Suyadnya

This study was intended to determine the free testosterone levels and sperm quality of local rabbit that was given commercial feed supplemented cod fish liver oil.  The experiment design that was used in this research was Complete Random Design (CRD) with four experiments of feed, i.e. commercial feed without cod fish liver oil (R-0) as control, commercial feed + 1,5% cod fish liver oil (R-1), commercial feed + cod fish liver oil 3% (R-2), commercial feed + cod fish liver oil 4,5% (R-3). The each experiment included eight rabbits and feed experiment was given starting by 13 weeks to 26 weeks years old. The variable that observed was free testosterone level and sperm quality of local rabbit. The data that was obtained to be analyzed with One Way Anova and if its contrast was done more test with Duncan’s Multiple Range Test (DMRT). The result of this research was to show that supplementation of cod fish liver oil in commercial feed was to show the result that a real distinction of (P<0, 05) towards free testosterone level and sperm quality of local rabbit.


2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Meng Zuo ◽  
Guotao Liao ◽  
Wenqian Zhang ◽  
Dan Xu ◽  
Juan Lu ◽  
...  

Abstract Objective PCOS is a heterogeneous endocrine disorder with both reproductive and metabolic abnormalities. At present, PCOS has been confirmed to have a certain genetic background. Compared with healthy women, the vast majority of PCOS patients have hyperandrogenemia, and this excessive androgen exposure during pregnancy may affect the development of female fetuses. The aim of the current study was to investigate the effect of adiponectin intervention during early pregnancy of obese mice with PCOS on the metabolic phenotype of adult female offspring. Methods After the PCOS model was established, C57BL/6J mice were divided into maternal-control, maternal-PCOS, and maternal-PCOS + APN groups. DHEA-induced PCOS mice were supplemented with adiponectin (10 mg/kg/day) in the early pregnancy in order to eliminate adverse hormone exposure and then traced for endocrine indicators in their adult female offspring, which were observed for metabolism syndrome or endocrine disturbance and exhibited the main effects of APN. To further explore the underlying mechanism, the relative expressions of phosphorylated AMPK, PI3K, and Akt were detected in the ovaries of offspring mice. Results The serum testosterone level of the maternal-PCOS + APN group in early pregnancy was significantly lower than that of the maternal-PCOS group (p < 0.01). The serum testosterone level in the offspring-PCOS + APN group was significantly lower than in the offspring-PCOS group (p <0.05), the diestrus time characterized by massive granulocyte aggregation in the estrus cycle was significantly shorter than in the offspring-PCOS group (p<0.05), and the phenotypes of PCOS-like reproductive disorders and metabolic disorders, such as obesity, insulin resistance, impaired glucose tolerance, and hyperlipidemia, were also significantly improved in the offspring-PCOS + APN group (p < 0.05). Compared with the control group, the expression levels of phosphorylated AMPK, PI3K, and Akt in the offspring-PCOS group were significantly decreased (p < 0.05), while those in the offspring-PCOS + APN group were significantly increased (p < 0.05). Conclusions APN intervention in early pregnancy significantly reduced the adverse effects of maternal obesity and high androgen levels during pregnancy on female offspring and corrected the PCOS-like endocrine phenotype and metabolic disorders of adult female offspring. This effect may be caused by the activation of the AMPK/PI3K-Akt signaling pathway in PCOS offspring mice.


2011 ◽  
Vol 144 (1-3) ◽  
pp. 264-271 ◽  
Author(s):  
Chung Soo Chang ◽  
Jong Bo Choi ◽  
Hae Jin Kim ◽  
Sat Byul Park

2002 ◽  
Vol 87 (3) ◽  
pp. 1129-1133 ◽  
Author(s):  
Johannes D. Veldhuis ◽  
George Zhang ◽  
James C. Garmey

Polycystic ovarian syndrome (anovulatory hyperandrogenism) is marked by adolescent onset of systemic hyperinsulinism, oligoovulation, hirsutism, excessive LH and androgen secretion, and variable reduction in fertility. Insulin and LH are believed to act in concert to promote ovarian androgen hypersecretion in this disorder. Administration of troglitazone, an insulin-sensitizing agent and putative PPARγ agonist, can decrease hyperinsulinism, suppress T production, and ameliorate oligoovulation in some women with this endocrinopathy. The present study tests the hypothesis that troglitazone directly inhibits de novo androgen biosynthesis stimulated jointly by LH and insulin in primary cultures of (porcine) thecal cells. We show that troglitazone dose-dependently antagonizes LH/insulin’s combined stimulation of androstenedione and T production by thecal cells in vitro. Consistent steroidogenic inhibition of 80–95% was achieved at drug concentrations of 3–6.8 μm (P &lt; 0.001). Exposure of thecal cells to the thiazolidinedione derivative also blocked bihormonally stimulated accumulation of CYP17 (cytochrome P450 17 α-hydroxylase/C17–20 lyase) gene expression, as reflected by decreased accumulation of cognate heterogeneous nuclear RNA and mRNA (by 30–65%; P &lt; 0.05). Moreover, troglitazone suppressed LH/insulin-induced phosphorylation of the 52-kDa immunoprecipitated CYP17 enzyme by 88% (P &lt; 0.001). A putative natural agonist of PPARγ nuclear transcription, 15-deoxy-δ-12,14-prostaglandin J2, also inhibited LH/insulin-driven androstenedione biosynthesis and CYP17 gene expression in thecal cells. In conclusion, a synthetic thiazolidinedione (troglitazone) and a natural ligand of PPARγ (15-deoxy-δ-12,14-prostaglandin J2) effectively impede the concerted stimulation by LH and insulin of in vitro thecal cell androgen production, CYP17 gene expression, and CYP17 protein phosphorylation. This ensemble of inhibitory actions on LH/insulin-stimulated steroidogenesis offers a plausible mechanistic basis for at least part of the observed clinical efficacy of troglitazone in mitigating androgen excess in women with polycystic ovarian syndrome.


2010 ◽  
Vol 183 (4S) ◽  
Author(s):  
Eduardo García-Cruz ◽  
Jorge Huguet Pérez ◽  
María José Ribal Caparrós ◽  
Meritxell Pérez Márquez ◽  
Marta Piqueras Bartolomé ◽  
...  

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