2000
DOI: 10.1210/en.141.11.4295
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Estrogen Deficiency, Obesity, and Skeletal Abnormalities in Follicle-Stimulating Hormone Receptor Knockout (FORKO) Female Mice

Abstract: Targeted disruption of the receptor for glycoprotein hormone, FSH (FSH-R) causes a gene dose-related endocrine and gametogenic abnormality in female mice. The resulting FSH-R knockout (FORKO) mutants have disordered estrous cycles, ovulatory defects, and atrophic uterus. The heterozygous animals that initially show reduced fertility undergo early reproductive senescence and stop breeding altogether. Lack of FSH-R signaling in females causes severe ovarian underdevelopment producing chronic estrogen deficiency.… Show more

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Cited by 99 publications
(140 citation statements)
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“…Aromatase-deficient mice (ArKO) develop increased fat pad mass, hyperinsulinemia, hyperlipidemia, and liver steatosis (Jones et al 2000). Mice deficient of follicle-stimulating hormone receptor show increased development of visceral fat (Danilovich et al 2000). Collectively, the majority of studies suggest that estrogen attenuates adipocyte development.…”
Section: Steroid Hormonesmentioning
confidence: 99%
“…Aromatase-deficient mice (ArKO) develop increased fat pad mass, hyperinsulinemia, hyperlipidemia, and liver steatosis (Jones et al 2000). Mice deficient of follicle-stimulating hormone receptor show increased development of visceral fat (Danilovich et al 2000). Collectively, the majority of studies suggest that estrogen attenuates adipocyte development.…”
Section: Steroid Hormonesmentioning
confidence: 99%
“…Flow cytometric evaluation of germ cells revealed a significant increase in the percentage of spermatogonia and nongerm cells whereas there was a significant decrease in elongated spermatids. Defects in sperm head shape, chromatin condensation and chromatin remodeling were also observed (Krishnamurthy et al 2000, Xing et al 2003. During the prepubertal period, the expression of transition proteins and protamine-2 was greatly diminished leading to delayed spermatogenesis.…”
Section: Male Reproductive Phenotypes In Forko Micementioning
confidence: 99%
“…FSHβ and FSH receptor (FSHR) knockout mice do not undergo bone loss after ovariectomy, 35 nor do rats that have been both hypophysectomized and ovariectomized, 36 supporting the idea that FSH is mainly responsible for ovariectomy-induced bone loss. However, complicating the in vivo analysis, the FSHR knockout mice have an increased level of testosterone, 37 and testosterone (via aromatization to estrogen or testosterone itself ) is protective of bone. 38 Despite the effects of testosterone, FSH acts, in part, directly on osteoclasts, as osteoclasts express the FSH receptor, and respond to FSH in vitro to activate osteoclastogenesis.…”
Section: Erα Knockout Mice Have Low Cortical Bone Mineral Densitymentioning
confidence: 99%