Activation of membrane-associated estrogen receptors decreases food and water intake in ovariectomized rats.
Identifieur interne : 002060 ( Main/Curation ); précédent : 002059; suivant : 002061Activation of membrane-associated estrogen receptors decreases food and water intake in ovariectomized rats.
Auteurs : Jessica Santollo [États-Unis] ; Anik Marshall ; Derek DanielsSource :
- Endocrinology [ 1945-7170 ] ; 2013.
Descripteurs français
- KwdFr :
- MESH :
- administration et posologie : Oestradiol.
- métabolisme : Récepteurs des oestrogènes.
- pharmacologie : Oestradiol.
- Animaux, Consommation alimentaire, Consommation de boisson, Femelle, Ovariectomie, Rat Long-Evans, Rats.
English descriptors
- KwdEn :
- MESH :
- chemical , administration & dosage : Estradiol.
- drug effects : Drinking, Eating.
- chemical , metabolism : Receptors, Estrogen.
- chemical , pharmacology : Estradiol.
- Animals, Female, Ovariectomy, Rats, Rats, Long-Evans.
Abstract
Estradiol (E2) decreases food and water intake in a variety of species, including rats. Available evidence suggests that this is mediated by genomic mechanisms that are most often attributed to nuclear estrogen receptors. More recent studies indicate that membrane-associated estrogen receptors (mERs) also can influence gene expression through the activation of transcription factors, yet it is unclear whether mERs are involved in mediating the hypophagic and antidipsetic effects of E2. In the present experiments, we injected E2 or a membrane-impermeable form of E2 (E2-BSA) into the lateral cerebral ventricle of ovariectomized female rats and evaluated the effect on 23 h food and water intake. First, we found that higher doses of E2 were necessary to reduce water intake than were sufficient to reduce food intake. Analysis of drinking microstructure revealed that the decrease in water intake after E2 treatment was mediated by both a decrease in burst number and burst size. Next, the activation of mERs with E2-BSA decreased both overnight food and water intake and analysis of drinking microstructure indicated that the decreased water intake resulted from a decrease in burst number. Finally, E2-BSA did not condition a taste aversion, suggesting that the inhibitory effects on food and water intake were not secondary to malaise. Together these findings suggest that activation of mERs is sufficient to decrease food and water intake in female rats.
DOI: 10.1210/en.2012-1858
PubMed: 23183173
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last="Marshall">Anik Marshall</name></author><author><name sortKey="Daniels, Derek" sort="Daniels, Derek" uniqKey="Daniels D" first="Derek" last="Daniels">Derek Daniels</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2013">2013</date><idno type="RBID">pubmed:23183173</idno><idno type="pmid">23183173</idno><idno type="doi">10.1210/en.2012-1858</idno><idno type="wicri:Area/PubMed/Corpus">001D36</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001D36</idno><idno type="wicri:Area/PubMed/Curation">001D36</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">001D36</idno><idno type="wicri:Area/PubMed/Checkpoint">001C07</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">001C07</idno><idno type="wicri:Area/Ncbi/Merge">000A08</idno><idno type="wicri:Area/Ncbi/Curation">000A08</idno><idno type="wicri:Area/Ncbi/Checkpoint">000A08</idno><idno 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Buffalo</orgName></affiliation></author><author><name sortKey="Marshall, Anik" sort="Marshall, Anik" uniqKey="Marshall A" first="Anik" last="Marshall">Anik Marshall</name></author><author><name sortKey="Daniels, Derek" sort="Daniels, Derek" uniqKey="Daniels D" first="Derek" last="Daniels">Derek Daniels</name></author></analytic><series><title level="j">Endocrinology</title><idno type="eISSN">1945-7170</idno><imprint><date when="2013" type="published">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Drinking (drug effects)</term><term>Eating (drug effects)</term><term>Estradiol (administration & dosage)</term><term>Estradiol (pharmacology)</term><term>Female</term><term>Ovariectomy</term><term>Rats</term><term>Rats, Long-Evans</term><term>Receptors, Estrogen (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Consommation alimentaire ()</term><term>Consommation de boisson ()</term><term>Femelle</term><term>Oestradiol (administration et posologie)</term><term>Oestradiol (pharmacologie)</term><term>Ovariectomie</term><term>Rat Long-Evans</term><term>Rats</term><term>Récepteurs des oestrogènes (métabolisme)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Estradiol</term></keywords><keywords scheme="MESH" qualifier="administration et posologie" xml:lang="fr"><term>Oestradiol</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Drinking</term><term>Eating</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Receptors, Estrogen</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Récepteurs des oestrogènes</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Oestradiol</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Estradiol</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Female</term><term>Ovariectomy</term><term>Rats</term><term>Rats, Long-Evans</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Consommation alimentaire</term><term>Consommation de boisson</term><term>Femelle</term><term>Ovariectomie</term><term>Rat Long-Evans</term><term>Rats</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Estradiol (E2) decreases food and water intake in a variety of species, including rats. Available evidence suggests that this is mediated by genomic mechanisms that are most often attributed to nuclear estrogen receptors. More recent studies indicate that membrane-associated estrogen receptors (mERs) also can influence gene expression through the activation of transcription factors, yet it is unclear whether mERs are involved in mediating the hypophagic and antidipsetic effects of E2. In the present experiments, we injected E2 or a membrane-impermeable form of E2 (E2-BSA) into the lateral cerebral ventricle of ovariectomized female rats and evaluated the effect on 23 h food and water intake. First, we found that higher doses of E2 were necessary to reduce water intake than were sufficient to reduce food intake. Analysis of drinking microstructure revealed that the decrease in water intake after E2 treatment was mediated by both a decrease in burst number and burst size. Next, the activation of mERs with E2-BSA decreased both overnight food and water intake and analysis of drinking microstructure indicated that the decreased water intake resulted from a decrease in burst number. Finally, E2-BSA did not condition a taste aversion, suggesting that the inhibitory effects on food and water intake were not secondary to malaise. Together these findings suggest that activation of mERs is sufficient to decrease food and water intake in female rats.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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