Perfluoroheptanoic acid induces Leydig cell hyperplasia but inhibits spermatogenesis in rats after pubertal exposure

Toxicology ◽  
2021 ◽  
Vol 448 ◽  
pp. 152633
Author(s):  
Zengqiang Li ◽  
Changchang Li ◽  
Zina Wen ◽  
Haoni Yan ◽  
Cheng Zou ◽  
...  
Keyword(s):  
Leydig Cell ◽  
Cell Hyperplasia ◽  
Leydig Cell Hyperplasia

scholarly journals Diffuse Stromal Leydig Cell Hyperplasia: A Unique Cause of Postmenopausal Hyperandrogenism and Virilization

2000 ◽  
Vol 75 (3) ◽  
pp. 288-292 ◽  
Author(s):  
Harris C. Taylor ◽  
Indira Pillay ◽  
Sebouh Setrakian
Keyword(s):  
Leydig Cell ◽  
Cell Hyperplasia ◽  
Leydig Cell Hyperplasia

Nodular Leydig cell hyperplasia in a boy with familial male-limited precocious puberty

2001 ◽  
Vol 138 (6) ◽  
pp. 949-951 ◽  
Author(s):  
Ellen Werber Leschek ◽  
Wai-Yee Chan ◽  
David A. Diamond ◽  
Martin Kaefer ◽  
Janet Jones ◽  
...  
Keyword(s):  
Precocious Puberty ◽  
Leydig Cell ◽  
Cell Hyperplasia ◽  
Leydig Cell Hyperplasia

scholarly journals Precocious Puberty and Leydig Cell Hyperplasia in Male Mice With a Gain of Function Mutation in the LH Receptor Gene

Endocrinology ◽  
2013 ◽  
Vol 154 (10) ◽  
pp. 3900-3913 ◽  
Author(s):  
Stacey R. McGee ◽  
Prema Narayan
Keyword(s):  
Mouse Model ◽  
Precocious Puberty ◽  
Leydig Cell ◽  
Receptor Gene ◽  
Fold Increase ◽  
Male Mice ◽  
Cell Hyperplasia ◽  
Lh Receptor ◽  
Genes Encoding ◽  
Leydig Cell Hyperplasia

The LH receptor (LHR) is critical for steroidogenesis and gametogenesis. Its essential role is underscored by the developmental and reproductive abnormalities that occur due to genetic mutations identified in the human LHR. In males, activating mutations are associated with precocious puberty and Leydig cell hyperplasia. To generate a mouse model for the human disease, we have introduced an aspartic acid to glycine mutation in amino acid residue 582 (D582G) of the mouse LHR gene corresponding to the most common D578G mutation found in boys with familial male-limited precocious puberty (FMPP). In transfected cells, mouse D582G mLHR exhibited constitutive activity with a 23-fold increase in basal cAMP levels compared with the wild-type receptor. A temporal study of male mice from 7 days to 24 weeks indicated that the knock-in mice with the mutated receptor (KiLHRD582G) exhibited precocious puberty with elevated testosterone levels as early as 7 days of age and through adulthood. Leydig cell-specific genes encoding LHR and several steroidogenic enzymes were up-regulated in KiLHRD582G testis. Leydig cell hyperplasia was detected at all ages, whereas Sertoli and germ cell development appeared normal. A novel finding from our studies, not previously reported in the FMPP cases, is that extensive hyperplasia is commonly found around the periphery of the testis. We further demonstrate that the hyperplasia is due to premature proliferation and precocious differentiation of adult Leydig cells in the KiLHRD582G testis. The KiLHRD582G mice provide a mouse model for FMPP, and we suggest that it is a useful model for studying pathologies associated with altered LHR signaling.

scholarly journals Ovarian Leydig Cell Hyperplasia: An Unusual Case of Virilization in a Postmenopausal Woman

2014 ◽  
Vol 2014 ◽  
pp. 1-4
Author(s):  
Jaya M. Mehta ◽  
Jeffrey L. Miller ◽  
Anthony J. Cannon ◽  
Stacey K. Mardekian ◽  
Lawrence C. Kenyon ◽  
...  
Keyword(s):  
Postmenopausal Woman ◽  
Medical History ◽  
Leydig Cell ◽  
Unusual Case ◽  
Serum Testosterone ◽  
Adrenal Tumors ◽  
Total Testosterone ◽  
Bilateral Oophorectomy ◽  
Cell Hyperplasia ◽  
Leydig Cell Hyperplasia

Objective. To report an unusual case of ovarian Leydig cell hyperplasia resulting in virilization in a postmenopausal woman.Methods. Patient’s medical history and pertinent literature were reviewed.Results. A 64-year-old woman presented with virilization with worsening hirsutism, deepening of her voice, male musculature, and male pattern alopecia. Her pertinent past medical history included type 1 diabetes, hyperlipidemia, and hypertension. Her pertinent past surgical history included hysterectomy due to fibroids. On further work-up, her serum total testosterone was 506 ng/dL (nl range: 2–45) and free testosterone was 40 pg/mL (nl range: 0.1–6.4). After ruling out adrenal causes, the patient underwent an empiric bilateral oophorectomy that showed Leydig cell hyperplasia on pathology. Six weeks postoperatively, serum testosterone was undetectable with significant clinical improvement.Conclusion. Postmenopausal hyperandrogenism can be the result of numerous etiologies ranging from normal physiologic changes to ovarian or rarely adrenal tumors. Our patient was found to have Leydig cell hyperplasia of her ovaries, a rarely reported cause of virilization.

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