Rodent Models for Human Polycystic Ovary Syndrome
Polycystic ovary syndrome (PCOS) is the most frequent female endocrine disorder, affecting 5%-10% of women, causing infertility due to dysfunctional follicular maturation and ovulation, distinctive multicystic ovaries and hyperandrogenism, together with metabolic abnormalities including obesity, hyp...
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Veröffentlicht in: | Biology of reproduction 2012-05, Vol.86 (5), p.149, 1-149 |
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description | Polycystic ovary syndrome (PCOS) is the most frequent female endocrine disorder, affecting 5%-10% of women, causing infertility due to dysfunctional follicular maturation and ovulation, distinctive multicystic ovaries and hyperandrogenism, together with metabolic abnormalities including obesity, hyperinsulinism, an increased risk of type 2 diabetes, and cardiovascular disease. The etiology of PCOS is unclear, and decisive clinical studies are limited by ethical and logistic constraints. Consequently treatment is palliative rather than curative and focuses on symptomatic approaches. Hence, a suitable animal model could provide a valuable means with which to study the pathogenesis of the characteristic reproductive and metabolic abnormalities and thereby identify novel and more effective treatments. So far there is no consensus on the best experimental animal model, which should ideally reproduce the key features associated with human PCOS. The prenatally androgenized rhesus monkey displays many characteristics of the human condition, including hyperandrogenism, anovulation, polycystic ovaries, increased adiposity, and insulin insensitivity. However, the high cost of nonhuman primate studies limits the practical utility of these large-animal models. Rodent models, on the other hand, are inexpensive, provide well-characterized and stable genetic backgrounds readily accessible for targeted genetic manipulation, and shorter reproductive life spans and generation times. Recent rodent models display both reproductive and metabolic disturbances associated with human PCOS. This review aimed to evaluate the rodent models reported to identify the advantages and disadvantages of the distinct rodent models used to investigate this complex endocrine disorder. |
doi_str_mv | 10.1095/biolreprod.111.097808 |
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The etiology of PCOS is unclear, and decisive clinical studies are limited by ethical and logistic constraints. Consequently treatment is palliative rather than curative and focuses on symptomatic approaches. Hence, a suitable animal model could provide a valuable means with which to study the pathogenesis of the characteristic reproductive and metabolic abnormalities and thereby identify novel and more effective treatments. So far there is no consensus on the best experimental animal model, which should ideally reproduce the key features associated with human PCOS. The prenatally androgenized rhesus monkey displays many characteristics of the human condition, including hyperandrogenism, anovulation, polycystic ovaries, increased adiposity, and insulin insensitivity. However, the high cost of nonhuman primate studies limits the practical utility of these large-animal models. Rodent models, on the other hand, are inexpensive, provide well-characterized and stable genetic backgrounds readily accessible for targeted genetic manipulation, and shorter reproductive life spans and generation times. Recent rodent models display both reproductive and metabolic disturbances associated with human PCOS. This review aimed to evaluate the rodent models reported to identify the advantages and disadvantages of the distinct rodent models used to investigate this complex endocrine disorder.</description><identifier>ISSN: 0006-3363</identifier><identifier>EISSN: 1529-7268</identifier><identifier>DOI: 10.1095/biolreprod.111.097808</identifier><identifier>PMID: 22337333</identifier><identifier>CODEN: BIREBV</identifier><language>eng</language><publisher>Madison, WI: Society for the Study of Reproduction</publisher><subject>Androgens - adverse effects ; Animals ; Aromatase Inhibitors - adverse effects ; Biological and medical sciences ; Disease Models, Animal ; Estrogens - adverse effects ; Female ; Fundamental and applied biological sciences. Psychology ; Humans ; Leptin - biosynthesis ; Leptin - genetics ; Luteinizing Hormone - biosynthesis ; Mice ; Mutation ; Obesity - genetics ; Obesity - metabolism ; Plasminogen Activator Inhibitor 1 - biosynthesis ; Plasminogen Activator Inhibitor 1 - genetics ; Polycystic Ovary Syndrome - chemically induced ; Polycystic Ovary Syndrome - genetics ; Polycystic Ovary Syndrome - metabolism ; Progestins - antagonists & inhibitors ; Rats ; Receptors, Leptin - biosynthesis ; Receptors, Leptin - genetics ; Vertebrates: reproduction</subject><ispartof>Biology of reproduction, 2012-05, Vol.86 (5), p.149, 1-149</ispartof><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c293t-16a3db3ee3b28eefe1a44c811487d5be5ce300f4da481182296eae21f3b4e65f3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=26259792$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22337333$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>WALTERS, Kirsty A</creatorcontrib><creatorcontrib>ALLAN, Charles M</creatorcontrib><creatorcontrib>HANDELSMAN, David J</creatorcontrib><title>Rodent Models for Human Polycystic Ovary Syndrome</title><title>Biology of reproduction</title><addtitle>Biol Reprod</addtitle><description>Polycystic ovary syndrome (PCOS) is the most frequent female endocrine disorder, affecting 5%-10% of women, causing infertility due to dysfunctional follicular maturation and ovulation, distinctive multicystic ovaries and hyperandrogenism, together with metabolic abnormalities including obesity, hyperinsulinism, an increased risk of type 2 diabetes, and cardiovascular disease. The etiology of PCOS is unclear, and decisive clinical studies are limited by ethical and logistic constraints. Consequently treatment is palliative rather than curative and focuses on symptomatic approaches. Hence, a suitable animal model could provide a valuable means with which to study the pathogenesis of the characteristic reproductive and metabolic abnormalities and thereby identify novel and more effective treatments. So far there is no consensus on the best experimental animal model, which should ideally reproduce the key features associated with human PCOS. The prenatally androgenized rhesus monkey displays many characteristics of the human condition, including hyperandrogenism, anovulation, polycystic ovaries, increased adiposity, and insulin insensitivity. However, the high cost of nonhuman primate studies limits the practical utility of these large-animal models. Rodent models, on the other hand, are inexpensive, provide well-characterized and stable genetic backgrounds readily accessible for targeted genetic manipulation, and shorter reproductive life spans and generation times. Recent rodent models display both reproductive and metabolic disturbances associated with human PCOS. This review aimed to evaluate the rodent models reported to identify the advantages and disadvantages of the distinct rodent models used to investigate this complex endocrine disorder.</description><subject>Androgens - adverse effects</subject><subject>Animals</subject><subject>Aromatase Inhibitors - adverse effects</subject><subject>Biological and medical sciences</subject><subject>Disease Models, Animal</subject><subject>Estrogens - adverse effects</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Humans</subject><subject>Leptin - biosynthesis</subject><subject>Leptin - genetics</subject><subject>Luteinizing Hormone - biosynthesis</subject><subject>Mice</subject><subject>Mutation</subject><subject>Obesity - genetics</subject><subject>Obesity - metabolism</subject><subject>Plasminogen Activator Inhibitor 1 - biosynthesis</subject><subject>Plasminogen Activator Inhibitor 1 - genetics</subject><subject>Polycystic Ovary Syndrome - chemically induced</subject><subject>Polycystic Ovary Syndrome - genetics</subject><subject>Polycystic Ovary Syndrome - metabolism</subject><subject>Progestins - antagonists & inhibitors</subject><subject>Rats</subject><subject>Receptors, Leptin - biosynthesis</subject><subject>Receptors, Leptin - genetics</subject><subject>Vertebrates: reproduction</subject><issn>0006-3363</issn><issn>1529-7268</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFz1tLxDAQBeAgiruu_gSlL4IvrZlMkiaPsqgrrKx4eS5pOoVKL2vTCv33Flzx6cDwcZjD2CXwBLhVt3nV1T3t-65IACDhNjXcHLElKGHjVGhzzJaccx0jalywsxA-OQeJAk_ZQgjEFBGXDF67gtohep6jDlHZ9dFmbFwbvXT15KcwVD7afbt-it6mtui7hs7ZSenqQBeHXLGPh_v39Sbe7h6f1nfb2AuLQwzaYZEjEebCEJUETkpvAKRJC5WT8oScl7Jwcj4aIawmRwJKzCVpVeKK3fz2zhu_RgpD1lTBU127lroxZMBBpDJVxs706kDHvKEi2_dVM7-c_c2cwfUBuOBdXfau9VX4d1oom1qBP3EVY0A</recordid><startdate>20120501</startdate><enddate>20120501</enddate><creator>WALTERS, Kirsty A</creator><creator>ALLAN, Charles M</creator><creator>HANDELSMAN, David J</creator><general>Society for the Study of Reproduction</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>20120501</creationdate><title>Rodent Models for Human Polycystic Ovary Syndrome</title><author>WALTERS, Kirsty A ; ALLAN, Charles M ; HANDELSMAN, David J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c293t-16a3db3ee3b28eefe1a44c811487d5be5ce300f4da481182296eae21f3b4e65f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Androgens - adverse effects</topic><topic>Animals</topic><topic>Aromatase Inhibitors - adverse effects</topic><topic>Biological and medical sciences</topic><topic>Disease Models, Animal</topic><topic>Estrogens - adverse effects</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Humans</topic><topic>Leptin - biosynthesis</topic><topic>Leptin - genetics</topic><topic>Luteinizing Hormone - biosynthesis</topic><topic>Mice</topic><topic>Mutation</topic><topic>Obesity - genetics</topic><topic>Obesity - metabolism</topic><topic>Plasminogen Activator Inhibitor 1 - biosynthesis</topic><topic>Plasminogen Activator Inhibitor 1 - genetics</topic><topic>Polycystic Ovary Syndrome - chemically induced</topic><topic>Polycystic Ovary Syndrome - genetics</topic><topic>Polycystic Ovary Syndrome - metabolism</topic><topic>Progestins - antagonists & inhibitors</topic><topic>Rats</topic><topic>Receptors, Leptin - biosynthesis</topic><topic>Receptors, Leptin - genetics</topic><topic>Vertebrates: reproduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>WALTERS, Kirsty A</creatorcontrib><creatorcontrib>ALLAN, Charles M</creatorcontrib><creatorcontrib>HANDELSMAN, David J</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>MEDLINE - Academic</collection><jtitle>Biology of reproduction</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>WALTERS, Kirsty A</au><au>ALLAN, Charles M</au><au>HANDELSMAN, David J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Rodent Models for Human Polycystic Ovary Syndrome</atitle><jtitle>Biology of reproduction</jtitle><addtitle>Biol Reprod</addtitle><date>2012-05-01</date><risdate>2012</risdate><volume>86</volume><issue>5</issue><spage>149, 1</spage><epage>149</epage><pages>149, 1-149</pages><issn>0006-3363</issn><eissn>1529-7268</eissn><coden>BIREBV</coden><abstract>Polycystic ovary syndrome (PCOS) is the most frequent female endocrine disorder, affecting 5%-10% of women, causing infertility due to dysfunctional follicular maturation and ovulation, distinctive multicystic ovaries and hyperandrogenism, together with metabolic abnormalities including obesity, hyperinsulinism, an increased risk of type 2 diabetes, and cardiovascular disease. The etiology of PCOS is unclear, and decisive clinical studies are limited by ethical and logistic constraints. Consequently treatment is palliative rather than curative and focuses on symptomatic approaches. Hence, a suitable animal model could provide a valuable means with which to study the pathogenesis of the characteristic reproductive and metabolic abnormalities and thereby identify novel and more effective treatments. So far there is no consensus on the best experimental animal model, which should ideally reproduce the key features associated with human PCOS. The prenatally androgenized rhesus monkey displays many characteristics of the human condition, including hyperandrogenism, anovulation, polycystic ovaries, increased adiposity, and insulin insensitivity. However, the high cost of nonhuman primate studies limits the practical utility of these large-animal models. Rodent models, on the other hand, are inexpensive, provide well-characterized and stable genetic backgrounds readily accessible for targeted genetic manipulation, and shorter reproductive life spans and generation times. Recent rodent models display both reproductive and metabolic disturbances associated with human PCOS. This review aimed to evaluate the rodent models reported to identify the advantages and disadvantages of the distinct rodent models used to investigate this complex endocrine disorder.</abstract><cop>Madison, WI</cop><pub>Society for the Study of Reproduction</pub><pmid>22337333</pmid><doi>10.1095/biolreprod.111.097808</doi><tpages>149</tpages></addata></record> |
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source | MEDLINE; Oxford University Press Journals All Titles (1996-Current); EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
subjects | Androgens - adverse effects Animals Aromatase Inhibitors - adverse effects Biological and medical sciences Disease Models, Animal Estrogens - adverse effects Female Fundamental and applied biological sciences. Psychology Humans Leptin - biosynthesis Leptin - genetics Luteinizing Hormone - biosynthesis Mice Mutation Obesity - genetics Obesity - metabolism Plasminogen Activator Inhibitor 1 - biosynthesis Plasminogen Activator Inhibitor 1 - genetics Polycystic Ovary Syndrome - chemically induced Polycystic Ovary Syndrome - genetics Polycystic Ovary Syndrome - metabolism Progestins - antagonists & inhibitors Rats Receptors, Leptin - biosynthesis Receptors, Leptin - genetics Vertebrates: reproduction |
title | Rodent Models for Human Polycystic Ovary Syndrome |
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