Suppression of growth hormone does not affect ongoing spermatogenesis in rats
Recent evidence suggests that growth hormone (GH) may enhance physiologic processes, such as spermatogenesis, in addition to causing classical anabolic effects. We have previously shown that testosterone restores spermatogenesis in rats that were made azoospermic by immunization against gonadotropin...
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| Veröffentlicht in: | Journal of andrology 1999-01, Vol.20 (1), p.102-108 |
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| creator | Awoniyi, C. A Veeramachaneni, D. N Roberts, D Tucker, K. E Chandrashekar, V Schlaff, W. D |
| description | Recent evidence suggests that growth hormone (GH) may enhance physiologic processes, such as spermatogenesis, in addition to causing classical anabolic effects. We have previously shown that testosterone restores spermatogenesis in rats that were made azoospermic by immunization against gonadotropin‐releasing hormone (GnRH). In this study, we investigated whether suppression of GH affects spermatogenesis and the ability of testosterone to restore spermatogenesis following immunization against GnRFI and/or growth hormone‐releasing hormone (GHRH). Twelve rats were actively immunized against GnRH (anti‐GnRH), twelve rats were actively immunized against GHRH (anti‐GHRH), six rats were immunized against both GnRH and GHRH (anti‐GnRH/GHRH), and six rats served as controls. Two weeks after the second booster, six rats each from the anti‐GnRH and anti‐GHRH groups as well as the six anti‐GnRH/GHRH rats received 24‐cm testosterone‐filled Silastic implants (1), and the remaining six rats from each of these groups received empty Silastic implants. All rats were euthanized 2 months later. Weights of testes and testicular sperm counts were determined Serum testosterone, luteinizing hormone (LH), follicle‐stimulating hormone (FSH), growth hormone (GH), and insulin‐like growth factor‐1 (IGF‐1) concentrations were determined by radioimmunoassays. Serum GH and IGF‐1 were suppressed in anti‐GHRH rats. IGF‐1 was partiallyrestored by testosterone in anti‐GHRH and in anti‐GnRH/GHRH rats, but GH was restored to control value in anti‐GnRH/GHRH rats. Serum LH and FSH were suppressed in anti‐GnRH and anti‐GnRH/GHRH rats, but only FSH was partially restored by testosterone. Suppression of GH did not affect maintenance of spermatogenesis. However, because 1 partially restored GH and IGF‐1 levels in anti‐GnRH/GHRH rats and because spermatogenesis was found to be restored in these rats, we conclude that GH does not play a role in the maintenance of spermatogenesis in adult rats, but it may be required for the replenishment of germ cells in experimentally induced regressed rat testes. |
| doi_str_mv | 10.1002/j.1939-4640.1999.tb02502.x |
| format | Article |
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A ; Veeramachaneni, D. N ; Roberts, D ; Tucker, K. E ; Chandrashekar, V ; Schlaff, W. D</creator><creatorcontrib>Awoniyi, C. A ; Veeramachaneni, D. N ; Roberts, D ; Tucker, K. E ; Chandrashekar, V ; Schlaff, W. D</creatorcontrib><description>Recent evidence suggests that growth hormone (GH) may enhance physiologic processes, such as spermatogenesis, in addition to causing classical anabolic effects. We have previously shown that testosterone restores spermatogenesis in rats that were made azoospermic by immunization against gonadotropin‐releasing hormone (GnRH). In this study, we investigated whether suppression of GH affects spermatogenesis and the ability of testosterone to restore spermatogenesis following immunization against GnRFI and/or growth hormone‐releasing hormone (GHRH). Twelve rats were actively immunized against GnRH (anti‐GnRH), twelve rats were actively immunized against GHRH (anti‐GHRH), six rats were immunized against both GnRH and GHRH (anti‐GnRH/GHRH), and six rats served as controls. Two weeks after the second booster, six rats each from the anti‐GnRH and anti‐GHRH groups as well as the six anti‐GnRH/GHRH rats received 24‐cm testosterone‐filled Silastic implants (1), and the remaining six rats from each of these groups received empty Silastic implants. All rats were euthanized 2 months later. Weights of testes and testicular sperm counts were determined Serum testosterone, luteinizing hormone (LH), follicle‐stimulating hormone (FSH), growth hormone (GH), and insulin‐like growth factor‐1 (IGF‐1) concentrations were determined by radioimmunoassays. Serum GH and IGF‐1 were suppressed in anti‐GHRH rats. IGF‐1 was partiallyrestored by testosterone in anti‐GHRH and in anti‐GnRH/GHRH rats, but GH was restored to control value in anti‐GnRH/GHRH rats. Serum LH and FSH were suppressed in anti‐GnRH and anti‐GnRH/GHRH rats, but only FSH was partially restored by testosterone. Suppression of GH did not affect maintenance of spermatogenesis. However, because 1 partially restored GH and IGF‐1 levels in anti‐GnRH/GHRH rats and because spermatogenesis was found to be restored in these rats, we conclude that GH does not play a role in the maintenance of spermatogenesis in adult rats, but it may be required for the replenishment of germ cells in experimentally induced regressed rat testes.</description><identifier>ISSN: 0196-3635</identifier><identifier>EISSN: 1939-4640</identifier><identifier>DOI: 10.1002/j.1939-4640.1999.tb02502.x</identifier><identifier>PMID: 10100480</identifier><identifier>CODEN: JOAND3</identifier><language>eng</language><publisher>Oxford, UK: Am Soc Andrology</publisher><subject>Animals ; Biological and medical sciences ; Body Weight ; Follicle Stimulating Hormone - blood ; follicle‐stimulating hormone (FSH) ; Fundamental and applied biological sciences. Psychology ; Growth Hormone - antagonists & inhibitors ; Growth Hormone - blood ; Growth Hormone - immunology ; Growth Hormone-Releasing Hormone - immunology ; Hormone metabolism and regulation ; Insulin-Like Growth Factor I - metabolism ; insulin‐like growth factor‐1 (IGF‐1) ; luteinizing hormone (LH) ; Luteinizing Hormone - blood ; Male ; Mammalian male genital system ; Organ Size ; Rats ; Rats, Sprague-Dawley ; Spermatogenesis - drug effects ; Testis - cytology ; Testosterone ; Testosterone - blood ; Testosterone - pharmacology ; Vertebrates: reproduction</subject><ispartof>Journal of andrology, 1999-01, Vol.20 (1), p.102-108</ispartof><rights>1999 American Society of Andrology</rights><rights>1999 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4832-eca7a6dfcdf66bb7bce002588fe97844ddd91d9e829cea5933cc94ce70ff24503</citedby><cites>FETCH-LOGICAL-c4832-eca7a6dfcdf66bb7bce002588fe97844ddd91d9e829cea5933cc94ce70ff24503</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fj.1939-4640.1999.tb02502.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fj.1939-4640.1999.tb02502.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1433,27924,27925,46409,46833</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1772097$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10100480$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Awoniyi, C. A</creatorcontrib><creatorcontrib>Veeramachaneni, D. N</creatorcontrib><creatorcontrib>Roberts, D</creatorcontrib><creatorcontrib>Tucker, K. E</creatorcontrib><creatorcontrib>Chandrashekar, V</creatorcontrib><creatorcontrib>Schlaff, W. D</creatorcontrib><title>Suppression of growth hormone does not affect ongoing spermatogenesis in rats</title><title>Journal of andrology</title><addtitle>J Androl</addtitle><description>Recent evidence suggests that growth hormone (GH) may enhance physiologic processes, such as spermatogenesis, in addition to causing classical anabolic effects. We have previously shown that testosterone restores spermatogenesis in rats that were made azoospermic by immunization against gonadotropin‐releasing hormone (GnRH). In this study, we investigated whether suppression of GH affects spermatogenesis and the ability of testosterone to restore spermatogenesis following immunization against GnRFI and/or growth hormone‐releasing hormone (GHRH). Twelve rats were actively immunized against GnRH (anti‐GnRH), twelve rats were actively immunized against GHRH (anti‐GHRH), six rats were immunized against both GnRH and GHRH (anti‐GnRH/GHRH), and six rats served as controls. Two weeks after the second booster, six rats each from the anti‐GnRH and anti‐GHRH groups as well as the six anti‐GnRH/GHRH rats received 24‐cm testosterone‐filled Silastic implants (1), and the remaining six rats from each of these groups received empty Silastic implants. All rats were euthanized 2 months later. Weights of testes and testicular sperm counts were determined Serum testosterone, luteinizing hormone (LH), follicle‐stimulating hormone (FSH), growth hormone (GH), and insulin‐like growth factor‐1 (IGF‐1) concentrations were determined by radioimmunoassays. Serum GH and IGF‐1 were suppressed in anti‐GHRH rats. IGF‐1 was partiallyrestored by testosterone in anti‐GHRH and in anti‐GnRH/GHRH rats, but GH was restored to control value in anti‐GnRH/GHRH rats. Serum LH and FSH were suppressed in anti‐GnRH and anti‐GnRH/GHRH rats, but only FSH was partially restored by testosterone. Suppression of GH did not affect maintenance of spermatogenesis. However, because 1 partially restored GH and IGF‐1 levels in anti‐GnRH/GHRH rats and because spermatogenesis was found to be restored in these rats, we conclude that GH does not play a role in the maintenance of spermatogenesis in adult rats, but it may be required for the replenishment of germ cells in experimentally induced regressed rat testes.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Body Weight</subject><subject>Follicle Stimulating Hormone - blood</subject><subject>follicle‐stimulating hormone (FSH)</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Growth Hormone - antagonists & inhibitors</subject><subject>Growth Hormone - blood</subject><subject>Growth Hormone - immunology</subject><subject>Growth Hormone-Releasing Hormone - immunology</subject><subject>Hormone metabolism and regulation</subject><subject>Insulin-Like Growth Factor I - metabolism</subject><subject>insulin‐like growth factor‐1 (IGF‐1)</subject><subject>luteinizing hormone (LH)</subject><subject>Luteinizing Hormone - blood</subject><subject>Male</subject><subject>Mammalian male genital system</subject><subject>Organ Size</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Spermatogenesis - drug effects</subject><subject>Testis - cytology</subject><subject>Testosterone</subject><subject>Testosterone - blood</subject><subject>Testosterone - pharmacology</subject><subject>Vertebrates: reproduction</subject><issn>0196-3635</issn><issn>1939-4640</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqVkMuO1DAQRS0EYpqBX0AWAnZp_MjLrBgNbw2wANaW45TTbiVxcKWVmb_HUVrAlpUt-9xbpUPIM872nDHx6rjnSqosL_P0oJTazw0TBRP723tk9-frPtkxrspMlrK4II8QjynLeCUfkgvOUlFesx358v00TREQfRhpcLSLYZkP9BDiEEagbQCkY5ipcQ7sTMPYBT92FCeIg5lDByOgR-pHGs2Mj8kDZ3qEJ-fzkvx8_-7H9cfs5tuHT9dXN5nNaykysKYyZets68qyaarGQtqtqGsHqqrzvG1bxVsFtVAWTKGktFblFirmnMgLJi_Jy613iuHXCXDWg0cLfW9GCCfUpSqLWrIVfL2BNgbECE5P0Q8m3mnO9CpTH_VqTK_G9CpTn2Xq2xR-ep5yagZo_4lu9hLw_AwYtKZ30YzW41-uqgRTVcLebNjie7j7jw3056uvb9drqnixVRx8d1h8BI2D6fu0GNfLsoiUTGVC_gbdX6BC</recordid><startdate>199901</startdate><enddate>199901</enddate><creator>Awoniyi, C. A</creator><creator>Veeramachaneni, D. N</creator><creator>Roberts, D</creator><creator>Tucker, K. E</creator><creator>Chandrashekar, V</creator><creator>Schlaff, W. D</creator><general>Am Soc Andrology</general><general>Blackwell Publishing Ltd</general><general>American Society of Andrology</general><scope>IQODW</scope><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>199901</creationdate><title>Suppression of growth hormone does not affect ongoing spermatogenesis in rats</title><author>Awoniyi, C. A ; Veeramachaneni, D. N ; Roberts, D ; Tucker, K. E ; Chandrashekar, V ; Schlaff, W. D</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4832-eca7a6dfcdf66bb7bce002588fe97844ddd91d9e829cea5933cc94ce70ff24503</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Body Weight</topic><topic>Follicle Stimulating Hormone - blood</topic><topic>follicle‐stimulating hormone (FSH)</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Growth Hormone - antagonists & inhibitors</topic><topic>Growth Hormone - blood</topic><topic>Growth Hormone - immunology</topic><topic>Growth Hormone-Releasing Hormone - immunology</topic><topic>Hormone metabolism and regulation</topic><topic>Insulin-Like Growth Factor I - metabolism</topic><topic>insulin‐like growth factor‐1 (IGF‐1)</topic><topic>luteinizing hormone (LH)</topic><topic>Luteinizing Hormone - blood</topic><topic>Male</topic><topic>Mammalian male genital system</topic><topic>Organ Size</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Spermatogenesis - drug effects</topic><topic>Testis - cytology</topic><topic>Testosterone</topic><topic>Testosterone - blood</topic><topic>Testosterone - pharmacology</topic><topic>Vertebrates: reproduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Awoniyi, C. A</creatorcontrib><creatorcontrib>Veeramachaneni, D. N</creatorcontrib><creatorcontrib>Roberts, D</creatorcontrib><creatorcontrib>Tucker, K. E</creatorcontrib><creatorcontrib>Chandrashekar, V</creatorcontrib><creatorcontrib>Schlaff, W. D</creatorcontrib><collection>Pascal-Francis</collection><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>Journal of andrology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Awoniyi, C. A</au><au>Veeramachaneni, D. N</au><au>Roberts, D</au><au>Tucker, K. E</au><au>Chandrashekar, V</au><au>Schlaff, W. D</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Suppression of growth hormone does not affect ongoing spermatogenesis in rats</atitle><jtitle>Journal of andrology</jtitle><addtitle>J Androl</addtitle><date>1999-01</date><risdate>1999</risdate><volume>20</volume><issue>1</issue><spage>102</spage><epage>108</epage><pages>102-108</pages><issn>0196-3635</issn><eissn>1939-4640</eissn><coden>JOAND3</coden><abstract>Recent evidence suggests that growth hormone (GH) may enhance physiologic processes, such as spermatogenesis, in addition to causing classical anabolic effects. We have previously shown that testosterone restores spermatogenesis in rats that were made azoospermic by immunization against gonadotropin‐releasing hormone (GnRH). In this study, we investigated whether suppression of GH affects spermatogenesis and the ability of testosterone to restore spermatogenesis following immunization against GnRFI and/or growth hormone‐releasing hormone (GHRH). Twelve rats were actively immunized against GnRH (anti‐GnRH), twelve rats were actively immunized against GHRH (anti‐GHRH), six rats were immunized against both GnRH and GHRH (anti‐GnRH/GHRH), and six rats served as controls. Two weeks after the second booster, six rats each from the anti‐GnRH and anti‐GHRH groups as well as the six anti‐GnRH/GHRH rats received 24‐cm testosterone‐filled Silastic implants (1), and the remaining six rats from each of these groups received empty Silastic implants. All rats were euthanized 2 months later. Weights of testes and testicular sperm counts were determined Serum testosterone, luteinizing hormone (LH), follicle‐stimulating hormone (FSH), growth hormone (GH), and insulin‐like growth factor‐1 (IGF‐1) concentrations were determined by radioimmunoassays. Serum GH and IGF‐1 were suppressed in anti‐GHRH rats. IGF‐1 was partiallyrestored by testosterone in anti‐GHRH and in anti‐GnRH/GHRH rats, but GH was restored to control value in anti‐GnRH/GHRH rats. Serum LH and FSH were suppressed in anti‐GnRH and anti‐GnRH/GHRH rats, but only FSH was partially restored by testosterone. Suppression of GH did not affect maintenance of spermatogenesis. However, because 1 partially restored GH and IGF‐1 levels in anti‐GnRH/GHRH rats and because spermatogenesis was found to be restored in these rats, we conclude that GH does not play a role in the maintenance of spermatogenesis in adult rats, but it may be required for the replenishment of germ cells in experimentally induced regressed rat testes.</abstract><cop>Oxford, UK</cop><pub>Am Soc Andrology</pub><pmid>10100480</pmid><doi>10.1002/j.1939-4640.1999.tb02502.x</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Biological and medical sciences Body Weight Follicle Stimulating Hormone - blood follicle‐stimulating hormone (FSH) Fundamental and applied biological sciences. Psychology Growth Hormone - antagonists & inhibitors Growth Hormone - blood Growth Hormone - immunology Growth Hormone-Releasing Hormone - immunology Hormone metabolism and regulation Insulin-Like Growth Factor I - metabolism insulin‐like growth factor‐1 (IGF‐1) luteinizing hormone (LH) Luteinizing Hormone - blood Male Mammalian male genital system Organ Size Rats Rats, Sprague-Dawley Spermatogenesis - drug effects Testis - cytology Testosterone Testosterone - blood Testosterone - pharmacology Vertebrates: reproduction |
| title | Suppression of growth hormone does not affect ongoing spermatogenesis in rats |
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