Kisspeptin in the Hypothalamus of 2 Rat Models of Polycystic Ovary Syndrome
Abstract Hyperandrogenism, disturbance of the hypothalamus-pituitary-ovary axis followed by elevated serum luteinizing hormone (LH) levels, and insulin resistance are involved in the complicated pathophysiology of polycystic ovary syndrome (PCOS). Kisspeptin is coexpressed with neurokinin B (NKB) in...
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| Veröffentlicht in: | Endocrinology (Philadelphia) 2017-02, Vol.158 (2), p.367-377 |
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| creator | Osuka, Satoko Iwase, Akira Nakahara, Tatsuo Kondo, Mika Saito, Ai Bayasula Nakamura, Tomoko Takikawa, Sachiko Goto, Maki Kotani, Tomomi Kikkawa, Fumitaka |
| description | Abstract
Hyperandrogenism, disturbance of the hypothalamus-pituitary-ovary axis followed by elevated serum luteinizing hormone (LH) levels, and insulin resistance are involved in the complicated pathophysiology of polycystic ovary syndrome (PCOS). Kisspeptin is coexpressed with neurokinin B (NKB) in the arcuate nucleus (ARC), the center of the gonadotropin-releasing hormone pulse generator that is responsible for pulsatile LH secretion. We compared 2 androgenized rat models of PCOS to evaluate the estrous cycle, hormonal profiles, and expression of kisspeptin and NKB in the ARC. Rats in our postnatal dihydrotestosterone (DHT)–treatment model exhibited weight gain and persistent diestrus with normal LH levels. In contrast, irregular cycles, with elevated LH serum levels and normal body weight, were found in the prenatally DHT-treated rats. We also found increased signals of kisspeptin and NKB in the ARC of the prenatally DHT-treated rats, and not in the postnatally DHT-treated rats. Our results suggest that prenatal exposure to androgens may result in higher kisspeptin and NKB levels in the ARC, which could be associated with 1 phenotype of PCOS that is characterized by normal body weight and higher LH secretion, whereas in postnatally DHT-treated rats, characteristics such as weight gain and normal LH levels are seen in the obese PCOS phenotype. |
| doi_str_mv | 10.1210/en.2016-1333 |
| format | Article |
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Hyperandrogenism, disturbance of the hypothalamus-pituitary-ovary axis followed by elevated serum luteinizing hormone (LH) levels, and insulin resistance are involved in the complicated pathophysiology of polycystic ovary syndrome (PCOS). Kisspeptin is coexpressed with neurokinin B (NKB) in the arcuate nucleus (ARC), the center of the gonadotropin-releasing hormone pulse generator that is responsible for pulsatile LH secretion. We compared 2 androgenized rat models of PCOS to evaluate the estrous cycle, hormonal profiles, and expression of kisspeptin and NKB in the ARC. Rats in our postnatal dihydrotestosterone (DHT)–treatment model exhibited weight gain and persistent diestrus with normal LH levels. In contrast, irregular cycles, with elevated LH serum levels and normal body weight, were found in the prenatally DHT-treated rats. We also found increased signals of kisspeptin and NKB in the ARC of the prenatally DHT-treated rats, and not in the postnatally DHT-treated rats. Our results suggest that prenatal exposure to androgens may result in higher kisspeptin and NKB levels in the ARC, which could be associated with 1 phenotype of PCOS that is characterized by normal body weight and higher LH secretion, whereas in postnatally DHT-treated rats, characteristics such as weight gain and normal LH levels are seen in the obese PCOS phenotype.</description><identifier>ISSN: 0013-7227</identifier><identifier>EISSN: 1945-7170</identifier><identifier>DOI: 10.1210/en.2016-1333</identifier><identifier>PMID: 27983870</identifier><language>eng</language><publisher>Washington, DC: Endocrine Society</publisher><subject>Androgens ; Animal models ; Animals ; Arcuate nucleus ; Arcuate Nucleus of Hypothalamus - metabolism ; Body Weight ; Body weight gain ; Dihydrotestosterone ; Disease Models, Animal ; Endocrinology ; Estrous Cycle ; Estrus cycle ; Female ; Gonadal Steroid Hormones - blood ; Gonadotropin-releasing hormone ; Gonadotropins ; Gonadotropins - blood ; Hypothalamo-Hypophyseal System - metabolism ; Hypothalamus ; Hypothalamus, Anterior - metabolism ; Insulin ; Insulin resistance ; Kiss1 protein ; Kisspeptins - metabolism ; Luteinizing hormone ; Neurokinin ; Neurokinin B ; Ovaries ; Ovary - metabolism ; Ovary - pathology ; Phenotype ; Phenotypes ; Pituitary ; Pituitary (anterior) ; Polycystic ovary syndrome ; Polycystic Ovary Syndrome - metabolism ; Polycystic Ovary Syndrome - pathology ; Prenatal experience ; Prenatal exposure ; Pulse generators ; Rats ; Rats, Wistar ; Rodents ; Secretion ; Serum levels ; Weight</subject><ispartof>Endocrinology (Philadelphia), 2017-02, Vol.158 (2), p.367-377</ispartof><rights>Copyright © 2017 by the Endocrine Society 2017</rights><rights>Copyright © 2017 by the Endocrine Society.</rights><rights>Copyright © 2017 Endocrine Society</rights><rights>Copyright © 2017 by the Endocrine Society</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27983870$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Osuka, Satoko</creatorcontrib><creatorcontrib>Iwase, Akira</creatorcontrib><creatorcontrib>Nakahara, Tatsuo</creatorcontrib><creatorcontrib>Kondo, Mika</creatorcontrib><creatorcontrib>Saito, Ai</creatorcontrib><creatorcontrib>Bayasula</creatorcontrib><creatorcontrib>Nakamura, Tomoko</creatorcontrib><creatorcontrib>Takikawa, Sachiko</creatorcontrib><creatorcontrib>Goto, Maki</creatorcontrib><creatorcontrib>Kotani, Tomomi</creatorcontrib><creatorcontrib>Kikkawa, Fumitaka</creatorcontrib><title>Kisspeptin in the Hypothalamus of 2 Rat Models of Polycystic Ovary Syndrome</title><title>Endocrinology (Philadelphia)</title><addtitle>Endocrinology</addtitle><description>Abstract
Hyperandrogenism, disturbance of the hypothalamus-pituitary-ovary axis followed by elevated serum luteinizing hormone (LH) levels, and insulin resistance are involved in the complicated pathophysiology of polycystic ovary syndrome (PCOS). Kisspeptin is coexpressed with neurokinin B (NKB) in the arcuate nucleus (ARC), the center of the gonadotropin-releasing hormone pulse generator that is responsible for pulsatile LH secretion. We compared 2 androgenized rat models of PCOS to evaluate the estrous cycle, hormonal profiles, and expression of kisspeptin and NKB in the ARC. Rats in our postnatal dihydrotestosterone (DHT)–treatment model exhibited weight gain and persistent diestrus with normal LH levels. In contrast, irregular cycles, with elevated LH serum levels and normal body weight, were found in the prenatally DHT-treated rats. We also found increased signals of kisspeptin and NKB in the ARC of the prenatally DHT-treated rats, and not in the postnatally DHT-treated rats. Our results suggest that prenatal exposure to androgens may result in higher kisspeptin and NKB levels in the ARC, which could be associated with 1 phenotype of PCOS that is characterized by normal body weight and higher LH secretion, whereas in postnatally DHT-treated rats, characteristics such as weight gain and normal LH levels are seen in the obese PCOS phenotype.</description><subject>Androgens</subject><subject>Animal models</subject><subject>Animals</subject><subject>Arcuate nucleus</subject><subject>Arcuate Nucleus of Hypothalamus - metabolism</subject><subject>Body Weight</subject><subject>Body weight gain</subject><subject>Dihydrotestosterone</subject><subject>Disease Models, Animal</subject><subject>Endocrinology</subject><subject>Estrous Cycle</subject><subject>Estrus cycle</subject><subject>Female</subject><subject>Gonadal Steroid Hormones - blood</subject><subject>Gonadotropin-releasing hormone</subject><subject>Gonadotropins</subject><subject>Gonadotropins - blood</subject><subject>Hypothalamo-Hypophyseal System - metabolism</subject><subject>Hypothalamus</subject><subject>Hypothalamus, Anterior - metabolism</subject><subject>Insulin</subject><subject>Insulin resistance</subject><subject>Kiss1 protein</subject><subject>Kisspeptins - metabolism</subject><subject>Luteinizing hormone</subject><subject>Neurokinin</subject><subject>Neurokinin B</subject><subject>Ovaries</subject><subject>Ovary - metabolism</subject><subject>Ovary - pathology</subject><subject>Phenotype</subject><subject>Phenotypes</subject><subject>Pituitary</subject><subject>Pituitary (anterior)</subject><subject>Polycystic ovary syndrome</subject><subject>Polycystic Ovary Syndrome - metabolism</subject><subject>Polycystic Ovary Syndrome - pathology</subject><subject>Prenatal experience</subject><subject>Prenatal exposure</subject><subject>Pulse generators</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Rodents</subject><subject>Secretion</subject><subject>Serum levels</subject><subject>Weight</subject><issn>0013-7227</issn><issn>1945-7170</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqN0UlLxTAQAOAgiu-53DxLwYNeqpkkzXKUhxs-UVzOJW2m2Efb1KYV-u-t68GDCAPDMB8DM0PIHtBjYEBPsDlmFGQMnPM1MgcjkliBoutkTinwWDGmZmQrhNVUCiH4JpkxZTTXis7J9XUZQottXzbRFP0zRpdj6_tnW9l6CJEvIhbd2z668Q6rj_rOV2M-hr7Mo9tX243Rw9i4zte4QzYKWwXc_crb5On87HFxGS9vL64Wp8t4JUD2sczzDJR1lhouHKdMJQ4LyVgCDJVz3BXaSCly0CikUTrjmNmiQKMl8AL5Njn6nNt2_mXA0Kd1GXKsKtugH0IK2oCWVLDkHzRh0lApYKIHv-jKD10zLZJy4FSBZlL8pcDoRKokUXpS-19qyGp0aduV9XSp9PvuEzj8BH5of7pA0_ePptikPx_lb-VrjUk</recordid><startdate>20170201</startdate><enddate>20170201</enddate><creator>Osuka, Satoko</creator><creator>Iwase, Akira</creator><creator>Nakahara, Tatsuo</creator><creator>Kondo, Mika</creator><creator>Saito, Ai</creator><creator>Bayasula</creator><creator>Nakamura, Tomoko</creator><creator>Takikawa, Sachiko</creator><creator>Goto, Maki</creator><creator>Kotani, Tomomi</creator><creator>Kikkawa, Fumitaka</creator><general>Endocrine Society</general><general>Oxford University Press</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7QG</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>20170201</creationdate><title>Kisspeptin in the Hypothalamus of 2 Rat Models of Polycystic Ovary Syndrome</title><author>Osuka, Satoko ; Iwase, Akira ; Nakahara, Tatsuo ; Kondo, Mika ; Saito, Ai ; Bayasula ; Nakamura, Tomoko ; Takikawa, Sachiko ; Goto, Maki ; Kotani, Tomomi ; Kikkawa, Fumitaka</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-j416t-6ccb17ada0934d30275def622512e7dd3df89664c18e46978b3ebaffe98613fe3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Androgens</topic><topic>Animal models</topic><topic>Animals</topic><topic>Arcuate nucleus</topic><topic>Arcuate Nucleus of Hypothalamus - metabolism</topic><topic>Body Weight</topic><topic>Body weight gain</topic><topic>Dihydrotestosterone</topic><topic>Disease Models, Animal</topic><topic>Endocrinology</topic><topic>Estrous Cycle</topic><topic>Estrus cycle</topic><topic>Female</topic><topic>Gonadal Steroid Hormones - blood</topic><topic>Gonadotropin-releasing hormone</topic><topic>Gonadotropins</topic><topic>Gonadotropins - blood</topic><topic>Hypothalamo-Hypophyseal System - metabolism</topic><topic>Hypothalamus</topic><topic>Hypothalamus, Anterior - metabolism</topic><topic>Insulin</topic><topic>Insulin resistance</topic><topic>Kiss1 protein</topic><topic>Kisspeptins - metabolism</topic><topic>Luteinizing hormone</topic><topic>Neurokinin</topic><topic>Neurokinin B</topic><topic>Ovaries</topic><topic>Ovary - metabolism</topic><topic>Ovary - pathology</topic><topic>Phenotype</topic><topic>Phenotypes</topic><topic>Pituitary</topic><topic>Pituitary (anterior)</topic><topic>Polycystic ovary syndrome</topic><topic>Polycystic Ovary Syndrome - metabolism</topic><topic>Polycystic Ovary Syndrome - pathology</topic><topic>Prenatal experience</topic><topic>Prenatal exposure</topic><topic>Pulse generators</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Rodents</topic><topic>Secretion</topic><topic>Serum levels</topic><topic>Weight</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Osuka, Satoko</creatorcontrib><creatorcontrib>Iwase, Akira</creatorcontrib><creatorcontrib>Nakahara, Tatsuo</creatorcontrib><creatorcontrib>Kondo, Mika</creatorcontrib><creatorcontrib>Saito, Ai</creatorcontrib><creatorcontrib>Bayasula</creatorcontrib><creatorcontrib>Nakamura, Tomoko</creatorcontrib><creatorcontrib>Takikawa, Sachiko</creatorcontrib><creatorcontrib>Goto, Maki</creatorcontrib><creatorcontrib>Kotani, Tomomi</creatorcontrib><creatorcontrib>Kikkawa, Fumitaka</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>Animal Behavior Abstracts</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Endocrinology (Philadelphia)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Osuka, Satoko</au><au>Iwase, Akira</au><au>Nakahara, Tatsuo</au><au>Kondo, Mika</au><au>Saito, Ai</au><au>Bayasula</au><au>Nakamura, Tomoko</au><au>Takikawa, Sachiko</au><au>Goto, Maki</au><au>Kotani, Tomomi</au><au>Kikkawa, Fumitaka</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Kisspeptin in the Hypothalamus of 2 Rat Models of Polycystic Ovary Syndrome</atitle><jtitle>Endocrinology (Philadelphia)</jtitle><addtitle>Endocrinology</addtitle><date>2017-02-01</date><risdate>2017</risdate><volume>158</volume><issue>2</issue><spage>367</spage><epage>377</epage><pages>367-377</pages><issn>0013-7227</issn><eissn>1945-7170</eissn><abstract>Abstract
Hyperandrogenism, disturbance of the hypothalamus-pituitary-ovary axis followed by elevated serum luteinizing hormone (LH) levels, and insulin resistance are involved in the complicated pathophysiology of polycystic ovary syndrome (PCOS). Kisspeptin is coexpressed with neurokinin B (NKB) in the arcuate nucleus (ARC), the center of the gonadotropin-releasing hormone pulse generator that is responsible for pulsatile LH secretion. We compared 2 androgenized rat models of PCOS to evaluate the estrous cycle, hormonal profiles, and expression of kisspeptin and NKB in the ARC. Rats in our postnatal dihydrotestosterone (DHT)–treatment model exhibited weight gain and persistent diestrus with normal LH levels. In contrast, irregular cycles, with elevated LH serum levels and normal body weight, were found in the prenatally DHT-treated rats. We also found increased signals of kisspeptin and NKB in the ARC of the prenatally DHT-treated rats, and not in the postnatally DHT-treated rats. Our results suggest that prenatal exposure to androgens may result in higher kisspeptin and NKB levels in the ARC, which could be associated with 1 phenotype of PCOS that is characterized by normal body weight and higher LH secretion, whereas in postnatally DHT-treated rats, characteristics such as weight gain and normal LH levels are seen in the obese PCOS phenotype.</abstract><cop>Washington, DC</cop><pub>Endocrine Society</pub><pmid>27983870</pmid><doi>10.1210/en.2016-1333</doi><tpages>11</tpages></addata></record> |
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| source | MEDLINE; Journals@Ovid Complete; Oxford University Press Journals All Titles (1996-Current); EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Androgens Animal models Animals Arcuate nucleus Arcuate Nucleus of Hypothalamus - metabolism Body Weight Body weight gain Dihydrotestosterone Disease Models, Animal Endocrinology Estrous Cycle Estrus cycle Female Gonadal Steroid Hormones - blood Gonadotropin-releasing hormone Gonadotropins Gonadotropins - blood Hypothalamo-Hypophyseal System - metabolism Hypothalamus Hypothalamus, Anterior - metabolism Insulin Insulin resistance Kiss1 protein Kisspeptins - metabolism Luteinizing hormone Neurokinin Neurokinin B Ovaries Ovary - metabolism Ovary - pathology Phenotype Phenotypes Pituitary Pituitary (anterior) Polycystic ovary syndrome Polycystic Ovary Syndrome - metabolism Polycystic Ovary Syndrome - pathology Prenatal experience Prenatal exposure Pulse generators Rats Rats, Wistar Rodents Secretion Serum levels Weight |
| title | Kisspeptin in the Hypothalamus of 2 Rat Models of Polycystic Ovary Syndrome |
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