scholarly journals Diverged Effects of Piperine on Testicular Development: Stimulating Leydig Cell Development but Inhibiting Spermatogenesis in Rats

2018 ◽  
Vol 9 ◽  
Author(s):  
Xianwu Chen ◽  
Fei Ge ◽  
Jianpeng Liu ◽  
Suhao Bao ◽  
Yong Chen ◽  
...  
2017 ◽  
Vol 8 ◽  
Author(s):  
Eddy Rijntjes ◽  
Marcos L. M. Gomes ◽  
Nina Zupanič ◽  
Hans J. M. Swarts ◽  
Jaap Keijer ◽  
...  

2021 ◽  
Vol 415 ◽  
pp. 115440
Author(s):  
Haoni Yan ◽  
Changchang Li ◽  
Cheng Zou ◽  
Xiu Xin ◽  
Xiaoheng Li ◽  
...  

2019 ◽  
Vol 10 ◽  
Author(s):  
Lanlan Chen ◽  
Xiaoheng Li ◽  
Yiyan Wang ◽  
Tiantian Song ◽  
Huitao Li ◽  
...  

1985 ◽  
Vol 121 (2) ◽  
pp. 99-109 ◽  
Author(s):  
R.L. Hullinger ◽  
C.J.G. Wensing
Keyword(s):  

1989 ◽  
Vol 100 (1) ◽  
pp. 62-85 ◽  
Author(s):  
Robert A. Anderson ◽  
Sally H. Berryman ◽  
Jack F. Phillips ◽  
Kenneth A. Feathergill ◽  
Lourens J.D. Zaneveld ◽  
...  

Endocrinology ◽  
2007 ◽  
Vol 148 (8) ◽  
pp. 3704-3710 ◽  
Author(s):  
Susan Y. Park ◽  
Minghan Tong ◽  
J. Larry Jameson

Testicular Leydig cells produce testosterone and provide the hormonal environment required for male virilization and spermatogenesis. In utero, fetal Leydig cells (FLCs) are necessary for the development of the Wolffian duct and male external genitalia. Steroidogenic factor 1 (Sf1) is a transcriptional regulator of hormone biosynthesis genes, thus serving a central role in the Leydig cell. Desert hedgehog (Dhh), a Sertoli cell product, specifies the FLC lineage in the primordial gonad through a paracrine signaling mechanism. Postnatally, FLCs are replaced in the testis by morphologically distinct adult Leydig cells (ALCs). To study a putative interaction between Sf1 and Dhh, we crossed Sf1 heterozygous mutant mice with Dhh homozygous null mice to test the function of these two genes in vivo. All of the compound Sf1+/−; Dhh−/− mutants failed to masculinize and were externally female. However, embryonic gonads contained anastomotic testis cords with Sertoli cells and germ cells, indicating that sex reversal was not attributable to a fate switch of the early gonad. Instead, external feminization was attributable to the absence of differentiated FLCs in XY compound mutant mice. ALCs also failed to develop, suggesting either a dependence of ALCs on the prenatal establishment of Leydig cell precursors or that Sf1 and Dhh are both required for ALC maturation. In summary, this study provides genetic evidence that combinatorial expression of the paracrine factor Dhh and nuclear transcription factor Sf1 is required for Leydig cell development.


Reproduction ◽  
2011 ◽  
Vol 141 (2) ◽  
pp. 217-225 ◽  
Author(s):  
Yasuhiro Kawai ◽  
Junko Noguchi ◽  
Kouyou Akiyama ◽  
Yuriko Takeno ◽  
Yasuhiro Fujiwara ◽  
...  

Development of the male gonads is a complex process with interaction of various cells in the gonads including germ, Sertoli, Leydig, and myoid cells. TF is a mutant rat strain showing male pseudohermaphroditism, with agenesis of Leydig cells and androgen deficiency controlled by an autosomal single recessive gene (mp). The mp locus was mapped on the distal region of rat chromosome 7 by linkage analysis, but the gene responsible for the mp mutation has not been identified. In this study, we performed fine linkage mapping and sequence analysis to determine the causative gene of the mp mutation, and performed an immunohistochemical study using a Leydig cell-specific marker to investigate detailed phenotypes of the mutant rats during the testicular development. As a result, we found a missense mutation of the gene encoding Desert hedgehog (Dhh) in the mutant rat, which could result in loss of function of the DHH signaling pathway. Histochemical examination revealed remarkably reduced number of fetal Leydig cells and lack of typical spindle-shaped adult Leydig cell in the mp/mp rats. These phenotypes resembled those of the Dhh-null mice. Additionally, testosterone levels were significantly lower in the mp/mp fetus, indicating androgen deficiency during embryonic development. These results indicate that the mutation of the Dhh gene may be responsible for the pseudohermaphrodite phenotypes of the mutant rat, and that the Dhh gene is probably essential for the development of Leydig cells.


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