endocrine/exocrine glands
• treatment with exogenous gonadotropins stimulated enlargement of the hypoplastic prostate glands
|
• treatment with exogenous gonadotropins stimulated enlargement of the hypoplastic seminal vesicles
|
• although ovarian follicles develop through the primary, secondary and antral stages, no large preovulatory follicles or corpora lutea are observed
• treatment with exogenous gonadotropins (PMSG) stimulated maturation of ovarian follicles to the preovulatory stage and induced ovulation, as indicated by the presence of corpora lutea
|
• severe
|
• mutant Leydig cells display none of the histological features typical of steroidogenic cells
|
• interstitial Leydig cells are severely reduced in number
• treatment with exogenous gonadotropins stimulated Leydig cell hypertrophy and induced luminal opening of the seminiferous tubules
|
• severe
|
cryptorchism
(
J:66593
)
• mutant males have cryptorchid testes
|
reproductive system
• male germ cells are significantly reduced in number
|
• although ovarian follicles develop through the primary, secondary and antral stages, no large preovulatory follicles or corpora lutea are observed
• treatment with exogenous gonadotropins (PMSG) stimulated maturation of ovarian follicles to the preovulatory stage and induced ovulation, as indicated by the presence of corpora lutea
|
• treatment with exogenous gonadotropins (PMSG) stimulated a significant increase in uterine size and development of the endometrial glands
|
• mutant males fail to progress through the normal stages of spermatogenesis: occasional pachytene spermatocytes are observed, but mature spermatids are absent
• treatment with exogenous gonadotropins (PMSG) stimulated gonadal steroidogenesis, inducing maturation of spermatogonial precursors to the round spermatid stage
|
• no mature spermatids are observed
|
• mutant males show hypoplastic external and internal genitalia
|
• treatment with exogenous gonadotropins stimulated enlargement of the hypoplastic prostate glands
|
• treatment with exogenous gonadotropins stimulated enlargement of the hypoplastic seminal vesicles
|
• mutant Leydig cells display none of the histological features typical of steroidogenic cells
|
• interstitial Leydig cells are severely reduced in number
• treatment with exogenous gonadotropins stimulated Leydig cell hypertrophy and induced luminal opening of the seminiferous tubules
|
cryptorchism
(
J:66593
)
• mutant males have cryptorchid testes
|
small gonad
(
J:66593
)
• mutant gonads are severely hypoplastic
|
• severe
|
• severe
|
• mutant vaginas fail to open at the normal age of puberty
|
• both male and female mutants are viable but fail to show signs of secondary sexual maturation, even at 6 months of age
• both male and female mutants exhibit sexual infantilism of the accessory sex organs
|
anovulation
(
J:66593
)
|
homeostasis/metabolism
• although mutant pituitaries appear histologically intact, immunoreactive FSH leves are virtually undetectable
• in contrast, pituitary ACTH, TSH and prolactin levels are comparable to those in wild-type pituitaries
|
• serum FSH levels are significantly reduced in both male and female mutants relative to wild-type controls
|
• although mutant pituitaries appear histologically intact, immunoreactive LH leves are virtually undetectable
|
• serum LH levels are significantly reduced in male mutants relative to wild-type controls
|
cellular
• no mature spermatids are observed
|
• male germ cells are significantly reduced in number
|
Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
hypogonadotropic hypogonadism | DOID:0090070 |
OMIM:PS147950 |
J:66593 |