What have gonadotrophin overexpressing transgenic mice taught us about gonadal function?
The two gonadotrophins, follicle-stimulating hormone and luteinising hormone, are pivotal regulators of the development and maintenance of normal fertility by maintaining testicular and ovarian endocrine function and gametogenesis. Too low gonadotrophin secretion, i.e. hypogonadotrophic hypogonadism...
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2005
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| Acceso en línea: | https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_14701626_v130_n3_p283_Rulli http://hdl.handle.net/20.500.12110/paper_14701626_v130_n3_p283_Rulli |
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paper:paper_14701626_v130_n3_p283_Rulli2023-06-08T16:17:03Z What have gonadotrophin overexpressing transgenic mice taught us about gonadal function? follitropin gonadotropin gonadotropin receptor luteinizing hormone tumor promoter climacterium endocrine function fertility gametogenesis gene mutation gene overexpression genetic analysis genetic model genital system disease gonad dysfunction gonad function gonadotropin release human hypogonadotropic hypogonadism hypophysis tumor infertility menopause mouse nonhuman ovary function ovary polycystic disease pathogenesis phenotype pregnancy priority journal review testis function transgenic mouse Animals Chorionic Gonadotropin Female Follicle Stimulating Hormone Gonadotropins, Pituitary Humans Luteinizing Hormone Male Mice Mice, Transgenic Models, Animal Ovary Reproduction Testis Mus musculus The two gonadotrophins, follicle-stimulating hormone and luteinising hormone, are pivotal regulators of the development and maintenance of normal fertility by maintaining testicular and ovarian endocrine function and gametogenesis. Too low gonadotrophin secretion, i.e. hypogonadotrophic hypogonadism, is a common cause of infertility. But there are also physiological and pathophysiological conditions where gonadotrophin secretion and/or action are either transiently or chronically elevated, such as pregnancy, pituitary tumours, polycystic ovarian syndrome, activating gonadotrophin receptor mutations, perimenopause and menopause. These situations can be either the primary or secondary cause of infertility and gonadal pathologies in both sexes. Also the role of gonadotrophins as tumour promoters is possible. Recently, the possibility to combine information from genetically modified mice and human phenotypes in connection with mutations of gonadotrophin or gonadotrophin receptor genes has elucidated many less well known mechanisms involved in dysregulation of gonadotrophin function. Among the genetically modified mouse models, transgenic mice with gonadotrophin hypersecretion have been developed during the last few years. In this review, we describe the key findings on transgenic mouse models overexpressing gonadotrophins and present their possible implications in related human pathologies. In addition, we provide examples of genetic mouse models with secondary effects on gonadotrophin production and, consequently, on gonadal function. © 2005 Society for Reproduction and Fertility. 2005 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_14701626_v130_n3_p283_Rulli http://hdl.handle.net/20.500.12110/paper_14701626_v130_n3_p283_Rulli |
| institution |
Universidad de Buenos Aires |
| institution_str |
I-28 |
| repository_str |
R-134 |
| collection |
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) |
| topic |
follitropin gonadotropin gonadotropin receptor luteinizing hormone tumor promoter climacterium endocrine function fertility gametogenesis gene mutation gene overexpression genetic analysis genetic model genital system disease gonad dysfunction gonad function gonadotropin release human hypogonadotropic hypogonadism hypophysis tumor infertility menopause mouse nonhuman ovary function ovary polycystic disease pathogenesis phenotype pregnancy priority journal review testis function transgenic mouse Animals Chorionic Gonadotropin Female Follicle Stimulating Hormone Gonadotropins, Pituitary Humans Luteinizing Hormone Male Mice Mice, Transgenic Models, Animal Ovary Reproduction Testis Mus musculus |
| spellingShingle |
follitropin gonadotropin gonadotropin receptor luteinizing hormone tumor promoter climacterium endocrine function fertility gametogenesis gene mutation gene overexpression genetic analysis genetic model genital system disease gonad dysfunction gonad function gonadotropin release human hypogonadotropic hypogonadism hypophysis tumor infertility menopause mouse nonhuman ovary function ovary polycystic disease pathogenesis phenotype pregnancy priority journal review testis function transgenic mouse Animals Chorionic Gonadotropin Female Follicle Stimulating Hormone Gonadotropins, Pituitary Humans Luteinizing Hormone Male Mice Mice, Transgenic Models, Animal Ovary Reproduction Testis Mus musculus What have gonadotrophin overexpressing transgenic mice taught us about gonadal function? |
| topic_facet |
follitropin gonadotropin gonadotropin receptor luteinizing hormone tumor promoter climacterium endocrine function fertility gametogenesis gene mutation gene overexpression genetic analysis genetic model genital system disease gonad dysfunction gonad function gonadotropin release human hypogonadotropic hypogonadism hypophysis tumor infertility menopause mouse nonhuman ovary function ovary polycystic disease pathogenesis phenotype pregnancy priority journal review testis function transgenic mouse Animals Chorionic Gonadotropin Female Follicle Stimulating Hormone Gonadotropins, Pituitary Humans Luteinizing Hormone Male Mice Mice, Transgenic Models, Animal Ovary Reproduction Testis Mus musculus |
| description |
The two gonadotrophins, follicle-stimulating hormone and luteinising hormone, are pivotal regulators of the development and maintenance of normal fertility by maintaining testicular and ovarian endocrine function and gametogenesis. Too low gonadotrophin secretion, i.e. hypogonadotrophic hypogonadism, is a common cause of infertility. But there are also physiological and pathophysiological conditions where gonadotrophin secretion and/or action are either transiently or chronically elevated, such as pregnancy, pituitary tumours, polycystic ovarian syndrome, activating gonadotrophin receptor mutations, perimenopause and menopause. These situations can be either the primary or secondary cause of infertility and gonadal pathologies in both sexes. Also the role of gonadotrophins as tumour promoters is possible. Recently, the possibility to combine information from genetically modified mice and human phenotypes in connection with mutations of gonadotrophin or gonadotrophin receptor genes has elucidated many less well known mechanisms involved in dysregulation of gonadotrophin function. Among the genetically modified mouse models, transgenic mice with gonadotrophin hypersecretion have been developed during the last few years. In this review, we describe the key findings on transgenic mouse models overexpressing gonadotrophins and present their possible implications in related human pathologies. In addition, we provide examples of genetic mouse models with secondary effects on gonadotrophin production and, consequently, on gonadal function. © 2005 Society for Reproduction and Fertility. |
| title |
What have gonadotrophin overexpressing transgenic mice taught us about gonadal function? |
| title_short |
What have gonadotrophin overexpressing transgenic mice taught us about gonadal function? |
| title_full |
What have gonadotrophin overexpressing transgenic mice taught us about gonadal function? |
| title_fullStr |
What have gonadotrophin overexpressing transgenic mice taught us about gonadal function? |
| title_full_unstemmed |
What have gonadotrophin overexpressing transgenic mice taught us about gonadal function? |
| title_sort |
what have gonadotrophin overexpressing transgenic mice taught us about gonadal function? |
| publishDate |
2005 |
| url |
https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_14701626_v130_n3_p283_Rulli http://hdl.handle.net/20.500.12110/paper_14701626_v130_n3_p283_Rulli |
| _version_ |
1768545111478632448 |