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Effects of low energy availability on female reproductive function
Background It is known that metabolic and nutritional disturbances induce reproductive dysfunction in females. The main cause of these alterations is reduced gonadotrophin‐releasing hormone (GnRH) secretion from the hypothalamus, and the underlying mechanisms have gradually been elucidated. Methods...
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Published in: | Reproductive medicine and biology 2022-01, Vol.21 (1), p.e12414-n/a |
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container_title | Reproductive medicine and biology |
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creator | Iwasa, Takeshi Minato, Saki Imaizumi, Junki Yoshida, Atsuko Kawakita, Takako Yoshida, Kanako Yamamoto, Yuri |
description | Background
It is known that metabolic and nutritional disturbances induce reproductive dysfunction in females. The main cause of these alterations is reduced gonadotrophin‐releasing hormone (GnRH) secretion from the hypothalamus, and the underlying mechanisms have gradually been elucidated.
Methods
The present review summarizes current knowledge about the effects of nutrition/metabolism on reproductive functions, especially focusing on the GnRH regulation system.
Main findings
Various central and peripheral factors are involved in the regulation of GnRH secretion, and alterations in their activity combine to affect GnRH neurons. Satiety‐related factors, i.e., leptin, insulin, and alpha‐melanocyte‐stimulating hormone, directly and indirectly stimulate GnRH secretion, whereas orexigenic factors, i.e., neuropeptide Y, Agouti‐related protein, orexin, and ghrelin, attenuate GnRH secretion. In addition, kisspeptin, which is a potent positive regulator of GnRH, expression is reduced by metabolic and nutritional disturbances.
Conclusion
These neuroendocrine systems may be defensive mechanisms, which help organisms to survive adverse conditions by temporarily suppressing reproduction. |
doi_str_mv | 10.1002/rmb2.12414 |
format | article |
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It is known that metabolic and nutritional disturbances induce reproductive dysfunction in females. The main cause of these alterations is reduced gonadotrophin‐releasing hormone (GnRH) secretion from the hypothalamus, and the underlying mechanisms have gradually been elucidated.
Methods
The present review summarizes current knowledge about the effects of nutrition/metabolism on reproductive functions, especially focusing on the GnRH regulation system.
Main findings
Various central and peripheral factors are involved in the regulation of GnRH secretion, and alterations in their activity combine to affect GnRH neurons. Satiety‐related factors, i.e., leptin, insulin, and alpha‐melanocyte‐stimulating hormone, directly and indirectly stimulate GnRH secretion, whereas orexigenic factors, i.e., neuropeptide Y, Agouti‐related protein, orexin, and ghrelin, attenuate GnRH secretion. In addition, kisspeptin, which is a potent positive regulator of GnRH, expression is reduced by metabolic and nutritional disturbances.
Conclusion
These neuroendocrine systems may be defensive mechanisms, which help organisms to survive adverse conditions by temporarily suppressing reproduction.</description><identifier>ISSN: 1445-5781</identifier><identifier>EISSN: 1447-0578</identifier><identifier>DOI: 10.1002/rmb2.12414</identifier><identifier>PMID: 34934398</identifier><language>eng</language><publisher>Japan: John Wiley & Sons, Inc</publisher><subject>Ablation ; Amenorrhea ; Appetite ; Energy ; Females ; Fertility ; Ghrelin ; GnRH ; Gonadotropin-releasing hormone ; Hormones ; Hypothalamus ; Hypotheses ; Infertility ; Insulin ; Kiss1 protein ; kisspeptin ; Leptin ; Metabolism ; Neuroendocrine system ; Neurons ; Neuropeptide Y ; Nutrition ; Nutritional status ; Orexins ; Peptides ; Pituitary (anterior) ; Puberty ; Review ; Satiety ; Secretion ; Weight control</subject><ispartof>Reproductive medicine and biology, 2022-01, Vol.21 (1), p.e12414-n/a</ispartof><rights>2021 The Authors. published by John Wiley & Sons Australia, Ltd on behalf of Japan Society for Reproductive Medicine.</rights><rights>2021 The Authors. Reproductive Medicine and Biology published by John Wiley & Sons Australia, Ltd on behalf of Japan Society for Reproductive Medicine.</rights><rights>2022. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c6044-fa69fed5d502fa58a2669a61c5f0758ace7deb84103344c8085fb914b5c442133</citedby><cites>FETCH-LOGICAL-c6044-fa69fed5d502fa58a2669a61c5f0758ace7deb84103344c8085fb914b5c442133</cites><orcidid>0000-0003-1014-5687</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2758333452/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2758333452?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,11560,25751,27922,27923,37010,37011,44588,46050,46474,53789,53791,74896</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34934398$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Iwasa, Takeshi</creatorcontrib><creatorcontrib>Minato, Saki</creatorcontrib><creatorcontrib>Imaizumi, Junki</creatorcontrib><creatorcontrib>Yoshida, Atsuko</creatorcontrib><creatorcontrib>Kawakita, Takako</creatorcontrib><creatorcontrib>Yoshida, Kanako</creatorcontrib><creatorcontrib>Yamamoto, Yuri</creatorcontrib><title>Effects of low energy availability on female reproductive function</title><title>Reproductive medicine and biology</title><addtitle>Reprod Med Biol</addtitle><description>Background
It is known that metabolic and nutritional disturbances induce reproductive dysfunction in females. The main cause of these alterations is reduced gonadotrophin‐releasing hormone (GnRH) secretion from the hypothalamus, and the underlying mechanisms have gradually been elucidated.
Methods
The present review summarizes current knowledge about the effects of nutrition/metabolism on reproductive functions, especially focusing on the GnRH regulation system.
Main findings
Various central and peripheral factors are involved in the regulation of GnRH secretion, and alterations in their activity combine to affect GnRH neurons. Satiety‐related factors, i.e., leptin, insulin, and alpha‐melanocyte‐stimulating hormone, directly and indirectly stimulate GnRH secretion, whereas orexigenic factors, i.e., neuropeptide Y, Agouti‐related protein, orexin, and ghrelin, attenuate GnRH secretion. In addition, kisspeptin, which is a potent positive regulator of GnRH, expression is reduced by metabolic and nutritional disturbances.
Conclusion
These neuroendocrine systems may be defensive mechanisms, which help organisms to survive adverse conditions by temporarily suppressing reproduction.</description><subject>Ablation</subject><subject>Amenorrhea</subject><subject>Appetite</subject><subject>Energy</subject><subject>Females</subject><subject>Fertility</subject><subject>Ghrelin</subject><subject>GnRH</subject><subject>Gonadotropin-releasing hormone</subject><subject>Hormones</subject><subject>Hypothalamus</subject><subject>Hypotheses</subject><subject>Infertility</subject><subject>Insulin</subject><subject>Kiss1 protein</subject><subject>kisspeptin</subject><subject>Leptin</subject><subject>Metabolism</subject><subject>Neuroendocrine system</subject><subject>Neurons</subject><subject>Neuropeptide Y</subject><subject>Nutrition</subject><subject>Nutritional status</subject><subject>Orexins</subject><subject>Peptides</subject><subject>Pituitary (anterior)</subject><subject>Puberty</subject><subject>Review</subject><subject>Satiety</subject><subject>Secretion</subject><subject>Weight control</subject><issn>1445-5781</issn><issn>1447-0578</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNp9kU1v1DAQhiMEoh9w4QegSFwQUlp_jBPngkSrllZqhYTgbDnOePHKiRc72Wr_Pe6mVC0HTh7bjx7P-C2Kd5ScUELYaRw6dkIZUHhRHFKApiKikS_3tahySQ-Ko5TWhNCmBfa6OODQcuCtPCzOLqxFM6Uy2NKHuxJHjKtdqbfaed0576ZdGcbS4qA9lhE3MfSzmdwWSzuPuQjjm-KV1T7h24f1uPh5efHj_Kq6-fb1-vzLTWVqAlBZXbcWe9ELwqwWUrO6bnVNjbCkyVuDTY-dBEo4BzCSSGG7lkInDACjnB8X14u3D3qtNtENOu5U0E7tD0JcKR0nZzwq3eSPybI8OoGs7mhvgIHtQef3pM6uz4trM3cD9gbHKWr_TPr8ZnS_1CpslaxFTSVkwccHQQy_Z0yTGlwy6L0eMcxJsZqypuE1Fxn98A-6DnMc81cplgfneVzBMvVpoUwMKUW0j81Qou5jVvcxq33MGX7_tP1H9G-uGaALcOc87v6jUt9vz9gi_QMJE7GQ</recordid><startdate>202201</startdate><enddate>202201</enddate><creator>Iwasa, Takeshi</creator><creator>Minato, Saki</creator><creator>Imaizumi, Junki</creator><creator>Yoshida, Atsuko</creator><creator>Kawakita, Takako</creator><creator>Yoshida, Kanako</creator><creator>Yamamoto, Yuri</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><general>Wiley</general><scope>24P</scope><scope>WIN</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>8FE</scope><scope>8FH</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0003-1014-5687</orcidid></search><sort><creationdate>202201</creationdate><title>Effects of low energy availability on female reproductive function</title><author>Iwasa, Takeshi ; Minato, Saki ; Imaizumi, Junki ; Yoshida, Atsuko ; Kawakita, Takako ; Yoshida, Kanako ; Yamamoto, Yuri</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c6044-fa69fed5d502fa58a2669a61c5f0758ace7deb84103344c8085fb914b5c442133</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Ablation</topic><topic>Amenorrhea</topic><topic>Appetite</topic><topic>Energy</topic><topic>Females</topic><topic>Fertility</topic><topic>Ghrelin</topic><topic>GnRH</topic><topic>Gonadotropin-releasing hormone</topic><topic>Hormones</topic><topic>Hypothalamus</topic><topic>Hypotheses</topic><topic>Infertility</topic><topic>Insulin</topic><topic>Kiss1 protein</topic><topic>kisspeptin</topic><topic>Leptin</topic><topic>Metabolism</topic><topic>Neuroendocrine system</topic><topic>Neurons</topic><topic>Neuropeptide Y</topic><topic>Nutrition</topic><topic>Nutritional status</topic><topic>Orexins</topic><topic>Peptides</topic><topic>Pituitary (anterior)</topic><topic>Puberty</topic><topic>Review</topic><topic>Satiety</topic><topic>Secretion</topic><topic>Weight control</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Iwasa, Takeshi</creatorcontrib><creatorcontrib>Minato, Saki</creatorcontrib><creatorcontrib>Imaizumi, Junki</creatorcontrib><creatorcontrib>Yoshida, Atsuko</creatorcontrib><creatorcontrib>Kawakita, Takako</creatorcontrib><creatorcontrib>Yoshida, Kanako</creatorcontrib><creatorcontrib>Yamamoto, Yuri</creatorcontrib><collection>Wiley-Blackwell Open Access Collection</collection><collection>Wiley Free Archive</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection (Proquest) (PQ_SDU_P3)</collection><collection>Biological Sciences</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database (Proquest) (PQ_SDU_P3)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>Directory of Open Access Journals</collection><jtitle>Reproductive medicine and biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Iwasa, Takeshi</au><au>Minato, Saki</au><au>Imaizumi, Junki</au><au>Yoshida, Atsuko</au><au>Kawakita, Takako</au><au>Yoshida, Kanako</au><au>Yamamoto, Yuri</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of low energy availability on female reproductive function</atitle><jtitle>Reproductive medicine and biology</jtitle><addtitle>Reprod Med Biol</addtitle><date>2022-01</date><risdate>2022</risdate><volume>21</volume><issue>1</issue><spage>e12414</spage><epage>n/a</epage><pages>e12414-n/a</pages><issn>1445-5781</issn><eissn>1447-0578</eissn><abstract>Background
It is known that metabolic and nutritional disturbances induce reproductive dysfunction in females. The main cause of these alterations is reduced gonadotrophin‐releasing hormone (GnRH) secretion from the hypothalamus, and the underlying mechanisms have gradually been elucidated.
Methods
The present review summarizes current knowledge about the effects of nutrition/metabolism on reproductive functions, especially focusing on the GnRH regulation system.
Main findings
Various central and peripheral factors are involved in the regulation of GnRH secretion, and alterations in their activity combine to affect GnRH neurons. Satiety‐related factors, i.e., leptin, insulin, and alpha‐melanocyte‐stimulating hormone, directly and indirectly stimulate GnRH secretion, whereas orexigenic factors, i.e., neuropeptide Y, Agouti‐related protein, orexin, and ghrelin, attenuate GnRH secretion. In addition, kisspeptin, which is a potent positive regulator of GnRH, expression is reduced by metabolic and nutritional disturbances.
Conclusion
These neuroendocrine systems may be defensive mechanisms, which help organisms to survive adverse conditions by temporarily suppressing reproduction.</abstract><cop>Japan</cop><pub>John Wiley & Sons, Inc</pub><pmid>34934398</pmid><doi>10.1002/rmb2.12414</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0003-1014-5687</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Ablation Amenorrhea Appetite Energy Females Fertility Ghrelin GnRH Gonadotropin-releasing hormone Hormones Hypothalamus Hypotheses Infertility Insulin Kiss1 protein kisspeptin Leptin Metabolism Neuroendocrine system Neurons Neuropeptide Y Nutrition Nutritional status Orexins Peptides Pituitary (anterior) Puberty Review Satiety Secretion Weight control |
title | Effects of low energy availability on female reproductive function |
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