Estrogen effects on oxytocinergic pathways that regulate food intake
Multiple stimulatory and inhibitory neural circuits control eating, and these circuits are influenced by an array of hormonal, neuropeptide, and neurotransmitter signals. For example, estrogen and oxytocin (OT) both are known to decrease food intake, but the mechanisms by which these signal molecule...
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| Veröffentlicht in: | Hormones and behavior 2018-09, Vol.105, p.128-137 |
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| description | Multiple stimulatory and inhibitory neural circuits control eating, and these circuits are influenced by an array of hormonal, neuropeptide, and neurotransmitter signals. For example, estrogen and oxytocin (OT) both are known to decrease food intake, but the mechanisms by which these signal molecules influence eating are not fully understood. These studies investigated the interaction between estrogen and OT in the control of food intake. RT-qPCR studies revealed that 17β-estradiol benzoate (EB)-treated rats showed a two-fold increase in OT mRNA in the paraventricular nucleus of the hypothalamus (PVN) compared to Oil-treated controls. Increased OT mRNA expression may increase OT protein levels, and immunohistochemistry studies showed that EB-treated rats had more intense OT labeling in the nucleus of the solitary tract (NTS), a region known to integrate signals for food intake. Food intake measurements showed that EB treatment reduced food intake, as expected. EB-treated rats lost weight over the course of the experiment, as expected, and EB-treated rats that received the highest dose of OT lost more weight than EB-treated rats that did not receive OT. Finally, OT antagonist administered to EB-treated rats reversed the effect of EB on food intake, suggesting that estrogen effects to decrease food intake may involve the oxytocinergic pathway.
•Oxytocin mRNA is increased in the paraventricular nucleus of the hypothalamus of EB-treated, ovariectomized rats•Oxytocin immunolabeling in the nucleus of the solitary tract is increased in EB-treated rats•Decreases in food intake and body weight are pronounced in EB-treated rats receiving ICV injections of oxytocin•EB-induced decreases in food intake are reversed with ICV administration of an oxytocin antagonist |
| doi_str_mv | 10.1016/j.yhbeh.2018.08.007 |
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•Oxytocin mRNA is increased in the paraventricular nucleus of the hypothalamus of EB-treated, ovariectomized rats•Oxytocin immunolabeling in the nucleus of the solitary tract is increased in EB-treated rats•Decreases in food intake and body weight are pronounced in EB-treated rats receiving ICV injections of oxytocin•EB-induced decreases in food intake are reversed with ICV administration of an oxytocin antagonist</description><identifier>ISSN: 0018-506X</identifier><identifier>EISSN: 1095-6867</identifier><identifier>DOI: 10.1016/j.yhbeh.2018.08.007</identifier><identifier>PMID: 30118729</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Appetite Regulation - drug effects ; Body weight ; Body Weight - drug effects ; Eating - drug effects ; Eating - physiology ; Estradiol - analogs & derivatives ; Estradiol - pharmacology ; Estrogens - pharmacology ; Female ; Hypothalamus - drug effects ; Hypothalamus - metabolism ; Intracerebroventricular injection ; Microstructural analysis ; Nucleus of the solitary tract ; Ovariectomy ; Oxytocin - genetics ; Oxytocin - metabolism ; Oxytocin - pharmacology ; Oxytocin antagonist ; Paraventricular Hypothalamic Nucleus - drug effects ; Paraventricular Hypothalamic Nucleus - metabolism ; Paraventricular nucleus ; Rats ; Rats, Sprague-Dawley ; Receptors, Oxytocin - antagonists & inhibitors ; Receptors, Oxytocin - genetics ; Receptors, Oxytocin - metabolism ; Signal Transduction - drug effects ; Signal Transduction - genetics ; Solitary Nucleus - drug effects ; Solitary Nucleus - metabolism</subject><ispartof>Hormones and behavior, 2018-09, Vol.105, p.128-137</ispartof><rights>2018 Elsevier Inc.</rights><rights>Copyright © 2018 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c359t-58e656583bd043667f174e0ae79d5240a29c3b90f06149c597c031044f18ba473</citedby><cites>FETCH-LOGICAL-c359t-58e656583bd043667f174e0ae79d5240a29c3b90f06149c597c031044f18ba473</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0018506X18302058$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65534</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30118729$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sloan, Dusti K.</creatorcontrib><creatorcontrib>Spencer, Diana S.</creatorcontrib><creatorcontrib>Curtis, Kathleen S.</creatorcontrib><title>Estrogen effects on oxytocinergic pathways that regulate food intake</title><title>Hormones and behavior</title><addtitle>Horm Behav</addtitle><description>Multiple stimulatory and inhibitory neural circuits control eating, and these circuits are influenced by an array of hormonal, neuropeptide, and neurotransmitter signals. For example, estrogen and oxytocin (OT) both are known to decrease food intake, but the mechanisms by which these signal molecules influence eating are not fully understood. These studies investigated the interaction between estrogen and OT in the control of food intake. RT-qPCR studies revealed that 17β-estradiol benzoate (EB)-treated rats showed a two-fold increase in OT mRNA in the paraventricular nucleus of the hypothalamus (PVN) compared to Oil-treated controls. Increased OT mRNA expression may increase OT protein levels, and immunohistochemistry studies showed that EB-treated rats had more intense OT labeling in the nucleus of the solitary tract (NTS), a region known to integrate signals for food intake. Food intake measurements showed that EB treatment reduced food intake, as expected. EB-treated rats lost weight over the course of the experiment, as expected, and EB-treated rats that received the highest dose of OT lost more weight than EB-treated rats that did not receive OT. Finally, OT antagonist administered to EB-treated rats reversed the effect of EB on food intake, suggesting that estrogen effects to decrease food intake may involve the oxytocinergic pathway.
•Oxytocin mRNA is increased in the paraventricular nucleus of the hypothalamus of EB-treated, ovariectomized rats•Oxytocin immunolabeling in the nucleus of the solitary tract is increased in EB-treated rats•Decreases in food intake and body weight are pronounced in EB-treated rats receiving ICV injections of oxytocin•EB-induced decreases in food intake are reversed with ICV administration of an oxytocin antagonist</description><subject>Animals</subject><subject>Appetite Regulation - drug effects</subject><subject>Body weight</subject><subject>Body Weight - drug effects</subject><subject>Eating - drug effects</subject><subject>Eating - physiology</subject><subject>Estradiol - analogs & derivatives</subject><subject>Estradiol - pharmacology</subject><subject>Estrogens - pharmacology</subject><subject>Female</subject><subject>Hypothalamus - drug effects</subject><subject>Hypothalamus - metabolism</subject><subject>Intracerebroventricular injection</subject><subject>Microstructural analysis</subject><subject>Nucleus of the solitary tract</subject><subject>Ovariectomy</subject><subject>Oxytocin - genetics</subject><subject>Oxytocin - metabolism</subject><subject>Oxytocin - pharmacology</subject><subject>Oxytocin antagonist</subject><subject>Paraventricular Hypothalamic Nucleus - drug effects</subject><subject>Paraventricular Hypothalamic Nucleus - metabolism</subject><subject>Paraventricular nucleus</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptors, Oxytocin - antagonists & inhibitors</subject><subject>Receptors, Oxytocin - genetics</subject><subject>Receptors, Oxytocin - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Signal Transduction - genetics</subject><subject>Solitary Nucleus - drug effects</subject><subject>Solitary Nucleus - metabolism</subject><issn>0018-506X</issn><issn>1095-6867</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1PwzAMhiMEgjH4BUioRy4dTpukzYED4luaxAUkblGaulvG1owkA_bvyRhwRLJkW37tV34IOaEwokDF-Wy0njY4HRVA6xGkgGqHDChInotaVLtkAGmScxAvB-QwhFlqKWdsnxyUqaqrQg7I9U2I3k2wz7Dr0MSQuT5zn-vojO3RT6zJljpOP_Q6ZHGqY-ZxsprriFnnXJvZPupXPCJ7nZ4HPP7JQ_J8e_N0dZ-PH-8eri7HuSm5jDmvUXDB67JpgZVCVB2tGILGSra8YKALacpGQgeCMmm4rAyUFBjraN1oVpVDcra9u_TubYUhqoUNBudz3aNbBVVALWsuBMgkLbdS410IHju19Hah_VpRUBt8aqa-8akNPgUpYGNw-mOwahbY_u388kqCi60A05vvFr0KxmJvsLU-0VOts_8afAEOE4D8</recordid><startdate>201809</startdate><enddate>201809</enddate><creator>Sloan, Dusti K.</creator><creator>Spencer, Diana S.</creator><creator>Curtis, Kathleen S.</creator><general>Elsevier Inc</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>201809</creationdate><title>Estrogen effects on oxytocinergic pathways that regulate food intake</title><author>Sloan, Dusti K. ; Spencer, Diana S. ; Curtis, Kathleen S.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c359t-58e656583bd043667f174e0ae79d5240a29c3b90f06149c597c031044f18ba473</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Animals</topic><topic>Appetite Regulation - drug effects</topic><topic>Body weight</topic><topic>Body Weight - drug effects</topic><topic>Eating - drug effects</topic><topic>Eating - physiology</topic><topic>Estradiol - analogs & derivatives</topic><topic>Estradiol - pharmacology</topic><topic>Estrogens - pharmacology</topic><topic>Female</topic><topic>Hypothalamus - drug effects</topic><topic>Hypothalamus - metabolism</topic><topic>Intracerebroventricular injection</topic><topic>Microstructural analysis</topic><topic>Nucleus of the solitary tract</topic><topic>Ovariectomy</topic><topic>Oxytocin - genetics</topic><topic>Oxytocin - metabolism</topic><topic>Oxytocin - pharmacology</topic><topic>Oxytocin antagonist</topic><topic>Paraventricular Hypothalamic Nucleus - drug effects</topic><topic>Paraventricular Hypothalamic Nucleus - metabolism</topic><topic>Paraventricular nucleus</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptors, Oxytocin - antagonists & inhibitors</topic><topic>Receptors, Oxytocin - genetics</topic><topic>Receptors, Oxytocin - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>Signal Transduction - genetics</topic><topic>Solitary Nucleus - drug effects</topic><topic>Solitary Nucleus - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sloan, Dusti K.</creatorcontrib><creatorcontrib>Spencer, Diana S.</creatorcontrib><creatorcontrib>Curtis, Kathleen S.</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 and behavior</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sloan, Dusti K.</au><au>Spencer, Diana S.</au><au>Curtis, Kathleen S.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Estrogen effects on oxytocinergic pathways that regulate food intake</atitle><jtitle>Hormones and behavior</jtitle><addtitle>Horm Behav</addtitle><date>2018-09</date><risdate>2018</risdate><volume>105</volume><spage>128</spage><epage>137</epage><pages>128-137</pages><issn>0018-506X</issn><eissn>1095-6867</eissn><abstract>Multiple stimulatory and inhibitory neural circuits control eating, and these circuits are influenced by an array of hormonal, neuropeptide, and neurotransmitter signals. For example, estrogen and oxytocin (OT) both are known to decrease food intake, but the mechanisms by which these signal molecules influence eating are not fully understood. These studies investigated the interaction between estrogen and OT in the control of food intake. RT-qPCR studies revealed that 17β-estradiol benzoate (EB)-treated rats showed a two-fold increase in OT mRNA in the paraventricular nucleus of the hypothalamus (PVN) compared to Oil-treated controls. Increased OT mRNA expression may increase OT protein levels, and immunohistochemistry studies showed that EB-treated rats had more intense OT labeling in the nucleus of the solitary tract (NTS), a region known to integrate signals for food intake. Food intake measurements showed that EB treatment reduced food intake, as expected. EB-treated rats lost weight over the course of the experiment, as expected, and EB-treated rats that received the highest dose of OT lost more weight than EB-treated rats that did not receive OT. Finally, OT antagonist administered to EB-treated rats reversed the effect of EB on food intake, suggesting that estrogen effects to decrease food intake may involve the oxytocinergic pathway.
•Oxytocin mRNA is increased in the paraventricular nucleus of the hypothalamus of EB-treated, ovariectomized rats•Oxytocin immunolabeling in the nucleus of the solitary tract is increased in EB-treated rats•Decreases in food intake and body weight are pronounced in EB-treated rats receiving ICV injections of oxytocin•EB-induced decreases in food intake are reversed with ICV administration of an oxytocin antagonist</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>30118729</pmid><doi>10.1016/j.yhbeh.2018.08.007</doi><tpages>10</tpages></addata></record> |
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| subjects | Animals Appetite Regulation - drug effects Body weight Body Weight - drug effects Eating - drug effects Eating - physiology Estradiol - analogs & derivatives Estradiol - pharmacology Estrogens - pharmacology Female Hypothalamus - drug effects Hypothalamus - metabolism Intracerebroventricular injection Microstructural analysis Nucleus of the solitary tract Ovariectomy Oxytocin - genetics Oxytocin - metabolism Oxytocin - pharmacology Oxytocin antagonist Paraventricular Hypothalamic Nucleus - drug effects Paraventricular Hypothalamic Nucleus - metabolism Paraventricular nucleus Rats Rats, Sprague-Dawley Receptors, Oxytocin - antagonists & inhibitors Receptors, Oxytocin - genetics Receptors, Oxytocin - metabolism Signal Transduction - drug effects Signal Transduction - genetics Solitary Nucleus - drug effects Solitary Nucleus - metabolism |
| title | Estrogen effects on oxytocinergic pathways that regulate food intake |
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