FSHβ knockout mouse model: a decade ago and into the future

Abstract

In 1997, more than 10 years ago now, we first reported the phenotypes of follicle stimulating hormone (FSH) β null mice. Since then, these mice have been useful for various physiological and genetic studies in reproductive biology. More recently, extra-gonadal functions of FSH have been discovered in bone. These studies opened up exciting avenues of new research on osteoporosis in postmenopausal women. Several genomics and proteomics tools and novel strategies to spatio-temporally restricting gene expression in vivo are available now. It is hoped that with the aid of these and other emerging technologies, an integrated network of FSH signaling pathways in various tissues would emerge in the near future. Undoubtedly, the coming 10 years should be more exciting to explore this “fertile” area of reproductive physiology research.

Genetic Analysis of Zebrafish Gonadotropin (FSH and LH) Functions by TALEN-Mediated Gene Disruption

“…It is likely that after the initial promotion by FSH to trigger male puberty in juveniles, the process of spermatogenesis becomes independent of pituitary gonadotrophic hormones. This agrees with a view in mammals that FSH plays a role in initiating spermatogenesis but not in maintaining the process in adults (4,60,61) although this concept still remains controversial (62). In FSH-deficient mice, the males are fertile but oligospermic with smaller testes (4), which agrees well with our finding in the zebrafish.…”

Luteotrophic effects of relaxin, chorionic gonadotrophin and FSH in common marmoset monkeys (Callithrix jacchus)

“…Thus, our results clearly demonstrate that FSH acts as a gonadotrophin with a luteotrophic effect, and that FSH has a function beyond its conventional allocation as a FSH only, as suggested by several authors, e.g. Kumar (2009). This assumption is supported by the detection of the FSH receptor in the human CL (Minegishi et al 1997).…”

Addition of recombinant follicle-stimulating hormone to human chorionic gonadotropin treatment in adolescents and young adults with hypogonadotropic hypogonadism promotes normal testicular growth and may promote early spermatogenesis

“…Intracytoplasmic sperm injection (ICSI) has been shown to be required to achieve fertility after failed gonadotropin treatment in men treated for the first time at ages 25 to 28 (12), and there is evidence that childhood FSH exposure may facilitate later spermatogenesis (13). Murine investigations in this area have limited applicability because spermatogenesis and fertility appear to be inducible and sustainable with testosterone alone in complete congenital gonadotropin deficiency (14)(15)(16) as well as in mice with either inactivating mutations of the FSH beta subunit gene (17) or the FSH receptor (18).…”