A short evolutionary history of FSH-stimulated spermatogenesis
It is well established in various experimental models that luteinizing hormone (LH) stimulated testosterone (T) production of Leydig cells is the key endocrine stimulus of spermatogenesis. The role of the other gonadotropin, follicle-stimulating hormone (FSH), is as yet somewhat unclear given that s...
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| Veröffentlicht in: | Hormones (Athens, Greece) Greece), 2015-10, Vol.14 (4), p.468-478 |
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| creator | Huhtaniemi, Ilpo |
| description | It is well established in various experimental models that luteinizing hormone (LH) stimulated testosterone (T) production of Leydig cells is the key endocrine stimulus of spermatogenesis. The role of the other gonadotropin, follicle-stimulating hormone (FSH), is as yet somewhat unclear given that several clinical conditions and experimental models, including men with inactivating
FSH receptor (R)
mutation and male
Fshb
and
Fshr
knockout mice, maintain fairly normal spermatogenesis and fertility. Furthermore, FSH treatment of male infertility has produced at best modest results. On the other hand, there are animal species (e.g. teleost fishes and the Djungarian hamster) where spermatogenesis is primarily FSH-dependent. The purpose of this article is to briefly review the gonadotrophin dependence of spermatogenesis in several model species and examine how it has shifted during evolution from FSH to LH dominance. The information may provide new insight into the role of FSH treatment of male infertility. |
| doi_str_mv | 10.14310/horm.2002.1632 |
| format | Article |
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FSH receptor (R)
mutation and male
Fshb
and
Fshr
knockout mice, maintain fairly normal spermatogenesis and fertility. Furthermore, FSH treatment of male infertility has produced at best modest results. On the other hand, there are animal species (e.g. teleost fishes and the Djungarian hamster) where spermatogenesis is primarily FSH-dependent. The purpose of this article is to briefly review the gonadotrophin dependence of spermatogenesis in several model species and examine how it has shifted during evolution from FSH to LH dominance. The information may provide new insight into the role of FSH treatment of male infertility.</description><identifier>ISSN: 1109-3099</identifier><identifier>EISSN: 2520-8721</identifier><identifier>DOI: 10.14310/horm.2002.1632</identifier><identifier>PMID: 26732152</identifier><language>eng</language><publisher>Cham: Springer International Publishing</publisher><subject>Animals ; Endocrinology ; Evolution, Molecular ; Fertility ; Follicle Stimulating Hormone - genetics ; Follicle Stimulating Hormone - metabolism ; Humans ; Infertility, Male - metabolism ; Infertility, Male - physiopathology ; Luteinizing Hormone - metabolism ; Male ; Medicine ; Medicine & Public Health ; Metabolic Diseases ; Models, Animal ; Polymorphism, Genetic ; Receptors, FSH - genetics ; Receptors, FSH - metabolism ; Review ; Signal Transduction ; Spermatogenesis ; Spermatozoa - metabolism ; Testosterone - metabolism</subject><ispartof>Hormones (Athens, Greece), 2015-10, Vol.14 (4), p.468-478</ispartof><rights>Hellenic Endocrine Society 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c445t-587bc5ae80b4a2a10ba4702bafd76fbb60fb743ba8a161a1e2ae6bbc4ccd2f093</citedby><cites>FETCH-LOGICAL-c445t-587bc5ae80b4a2a10ba4702bafd76fbb60fb743ba8a161a1e2ae6bbc4ccd2f093</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.14310/horm.2002.1632$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.14310/horm.2002.1632$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26732152$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Huhtaniemi, Ilpo</creatorcontrib><title>A short evolutionary history of FSH-stimulated spermatogenesis</title><title>Hormones (Athens, Greece)</title><addtitle>Hormones</addtitle><addtitle>Hormones (Athens)</addtitle><description>It is well established in various experimental models that luteinizing hormone (LH) stimulated testosterone (T) production of Leydig cells is the key endocrine stimulus of spermatogenesis. The role of the other gonadotropin, follicle-stimulating hormone (FSH), is as yet somewhat unclear given that several clinical conditions and experimental models, including men with inactivating
FSH receptor (R)
mutation and male
Fshb
and
Fshr
knockout mice, maintain fairly normal spermatogenesis and fertility. Furthermore, FSH treatment of male infertility has produced at best modest results. On the other hand, there are animal species (e.g. teleost fishes and the Djungarian hamster) where spermatogenesis is primarily FSH-dependent. The purpose of this article is to briefly review the gonadotrophin dependence of spermatogenesis in several model species and examine how it has shifted during evolution from FSH to LH dominance. The information may provide new insight into the role of FSH treatment of male infertility.</description><subject>Animals</subject><subject>Endocrinology</subject><subject>Evolution, Molecular</subject><subject>Fertility</subject><subject>Follicle Stimulating Hormone - genetics</subject><subject>Follicle Stimulating Hormone - metabolism</subject><subject>Humans</subject><subject>Infertility, Male - metabolism</subject><subject>Infertility, Male - physiopathology</subject><subject>Luteinizing Hormone - metabolism</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metabolic Diseases</subject><subject>Models, Animal</subject><subject>Polymorphism, Genetic</subject><subject>Receptors, FSH - genetics</subject><subject>Receptors, FSH - metabolism</subject><subject>Review</subject><subject>Signal Transduction</subject><subject>Spermatogenesis</subject><subject>Spermatozoa - metabolism</subject><subject>Testosterone - metabolism</subject><issn>1109-3099</issn><issn>2520-8721</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kDFPwzAQhS0EoqUws6GMLGnvHMdJFqSqohSpEgMwW3bitKmSuNgOEv8elxY2pjfcd096HyG3CFNkCcJsa2w3pQB0ijyhZ2RMUwpxnlE8J2NEKOIEimJErpzbAfC0yPGSjCjPEoopHZOHeeRCh4_0p2kH35he2q9o2zhvQpo6Wr6uYuebbmil11Xk9tp20puN7rVr3DW5qGXr9M0pJ-R9-fi2WMXrl6fnxXwdl4ylPk7zTJWp1DkoJqlEUJJlQJWsq4zXSnGoVcYSJXOJHCVqKjVXqmRlWdEaimRC7o-9e2s-Bu286BpX6raVvTaDE5hxxoucYhbQ2REtrXHO6lrsbdOFVQJB_EgTB2niIE0cpIWPu1P5oDpd_fG_lgIAR8CFU7_RVuzMYPsw-N_Ob-Y2eWA</recordid><startdate>20151001</startdate><enddate>20151001</enddate><creator>Huhtaniemi, Ilpo</creator><general>Springer International Publishing</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20151001</creationdate><title>A short evolutionary history of FSH-stimulated spermatogenesis</title><author>Huhtaniemi, Ilpo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c445t-587bc5ae80b4a2a10ba4702bafd76fbb60fb743ba8a161a1e2ae6bbc4ccd2f093</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Animals</topic><topic>Endocrinology</topic><topic>Evolution, Molecular</topic><topic>Fertility</topic><topic>Follicle Stimulating Hormone - genetics</topic><topic>Follicle Stimulating Hormone - metabolism</topic><topic>Humans</topic><topic>Infertility, Male - metabolism</topic><topic>Infertility, Male - physiopathology</topic><topic>Luteinizing Hormone - metabolism</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Metabolic Diseases</topic><topic>Models, Animal</topic><topic>Polymorphism, Genetic</topic><topic>Receptors, FSH - genetics</topic><topic>Receptors, FSH - metabolism</topic><topic>Review</topic><topic>Signal Transduction</topic><topic>Spermatogenesis</topic><topic>Spermatozoa - metabolism</topic><topic>Testosterone - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Huhtaniemi, Ilpo</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Hormones (Athens, Greece)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Huhtaniemi, Ilpo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A short evolutionary history of FSH-stimulated spermatogenesis</atitle><jtitle>Hormones (Athens, Greece)</jtitle><stitle>Hormones</stitle><addtitle>Hormones (Athens)</addtitle><date>2015-10-01</date><risdate>2015</risdate><volume>14</volume><issue>4</issue><spage>468</spage><epage>478</epage><pages>468-478</pages><issn>1109-3099</issn><eissn>2520-8721</eissn><abstract>It is well established in various experimental models that luteinizing hormone (LH) stimulated testosterone (T) production of Leydig cells is the key endocrine stimulus of spermatogenesis. The role of the other gonadotropin, follicle-stimulating hormone (FSH), is as yet somewhat unclear given that several clinical conditions and experimental models, including men with inactivating
FSH receptor (R)
mutation and male
Fshb
and
Fshr
knockout mice, maintain fairly normal spermatogenesis and fertility. Furthermore, FSH treatment of male infertility has produced at best modest results. On the other hand, there are animal species (e.g. teleost fishes and the Djungarian hamster) where spermatogenesis is primarily FSH-dependent. The purpose of this article is to briefly review the gonadotrophin dependence of spermatogenesis in several model species and examine how it has shifted during evolution from FSH to LH dominance. The information may provide new insight into the role of FSH treatment of male infertility.</abstract><cop>Cham</cop><pub>Springer International Publishing</pub><pmid>26732152</pmid><doi>10.14310/horm.2002.1632</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Hormones (Athens, Greece), 2015-10, Vol.14 (4), p.468-478 |
| issn | 1109-3099 2520-8721 |
| language | eng |
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| source | MEDLINE; SpringerNature Journals; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Animals Endocrinology Evolution, Molecular Fertility Follicle Stimulating Hormone - genetics Follicle Stimulating Hormone - metabolism Humans Infertility, Male - metabolism Infertility, Male - physiopathology Luteinizing Hormone - metabolism Male Medicine Medicine & Public Health Metabolic Diseases Models, Animal Polymorphism, Genetic Receptors, FSH - genetics Receptors, FSH - metabolism Review Signal Transduction Spermatogenesis Spermatozoa - metabolism Testosterone - metabolism |
| title | A short evolutionary history of FSH-stimulated spermatogenesis |
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