Abstract:
:LH and FSH act on gonadal cells to regulate steroidogenesis and gametogenesis. To model human reproductive disorders involving loss of LH function and to define LH-responsive genes, we produced knockout mice lacking the hormone-specific LHbeta subunit. LHbeta null mice are viable but demonstrate postnatal defects in gonadal growth and function resulting in infertility. Mutant males have decreased testes size, a block in Leydig cell differentiation, and a reduction in serum and intra-testicular testosterone levels. Furthermore, spermatogenesis is blocked at the round spermatid stage resulting in a total absence of the elongated spermatids. Mutant female mice are hypogonadal and demonstrate decreased levels of serum estradiol and progesterone. Ovarian histology reveals normal thecal layer, defects in folliculogenesis including many degenerating antral follicles and absence of corpora lutea. The defects in both sexes are not secondary to aberrant FSH regulation, since FSH levels were unaffected in null mice. Finally, the null mice can be pharmacologically rescued by exogenous hCG indicating that LH-responsiveness of the target cells is not irreversibly lost. Thus, LHbeta null mice provide a useful model to study the consequences of an isolated deficiency of LH ligand in reproduction, while retaining normal LH-responsiveness in target cells.
journal_name
Mol Cell Endocrinoljournal_title
Molecular and cellular endocrinologyauthors
Kumar TRdoi
10.1016/j.mce.2006.10.020subject
Has Abstractpub_date
2007-04-15 00:00:00pages
81-4issue
1-2eissn
0303-7207issn
1872-8057pii
S0303-7207(07)00051-2journal_volume
269pub_type
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