The use of animal models to decipher physiological and neurobiological alterations of anorexia nervosa patients.
Identifieur interne : 000252 ( PubMed/Checkpoint ); précédent : 000251; suivant : 000253The use of animal models to decipher physiological and neurobiological alterations of anorexia nervosa patients.
Auteurs : Mathieu Méquinion [France] ; Christophe Chauveau [France] ; Odile Viltart [France]Source :
- Frontiers in endocrinology ; 2015.
Abstract
Extensive studies were performed to decipher the mechanisms regulating feeding due to the worldwide obesity pandemy and its complications. The data obtained might be adapted to another disorder related to alteration of food intake, the restrictive anorexia nervosa. This multifactorial disease with a complex and unknown etiology is considered as an awful eating disorder since the chronic refusal to eat leads to severe, and sometimes, irreversible complications for the whole organism, until death. There is an urgent need to better understand the different aspects of the disease to develop novel approaches complementary to the usual psychological therapies. For this purpose, the use of pertinent animal models becomes a necessity. We present here the various rodent models described in the literature that might be used to dissect central and peripheral mechanisms involved in the adaptation to deficient energy supplies and/or the maintenance of physiological alterations on the long term. Data obtained from the spontaneous or engineered genetic models permit to better apprehend the implication of one signaling system (hormone, neuropeptide, neurotransmitter) in the development of several symptoms observed in anorexia nervosa. As example, mutations in the ghrelin, serotonin, dopamine pathways lead to alterations that mimic the phenotype, but compensatory mechanisms often occur rendering necessary the use of more selective gene strategies. Until now, environmental animal models based on one or several inducing factors like diet restriction, stress, or physical activity mimicked more extensively central and peripheral alterations decribed in anorexia nervosa. They bring significant data on feeding behavior, energy expenditure, and central circuit alterations. Animal models are described and criticized on the basis of the criteria of validity for anorexia nervosa.
DOI: 10.3389/fendo.2015.00068
PubMed: 26042085
Affiliations:
Links toward previous steps (curation, corpus...)
Links to Exploration step
pubmed:26042085Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">The use of animal models to decipher physiological and neurobiological alterations of anorexia nervosa patients.</title><author><name sortKey="Mequinion, Mathieu" sort="Mequinion, Mathieu" uniqKey="Mequinion M" first="Mathieu" last="Méquinion">Mathieu Méquinion</name><affiliation wicri:level="1"><nlm:affiliation>INSERM UMR-S1172, Development and Plasticity of Postnatal Brain , Lille , France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>INSERM UMR-S1172, Development and Plasticity of Postnatal Brain , Lille </wicri:regionArea><wicri:noRegion>Lille </wicri:noRegion><wicri:noRegion>Lille </wicri:noRegion></affiliation></author><author><name sortKey="Chauveau, Christophe" sort="Chauveau, Christophe" uniqKey="Chauveau C" first="Christophe" last="Chauveau">Christophe Chauveau</name><affiliation wicri:level="1"><nlm:affiliation>Pathophysiology of Inflammatory Bone Diseases, EA 4490, University of the Littoral Opal Coast , Boulogne sur Mer , France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Pathophysiology of Inflammatory Bone Diseases, EA 4490, University of the Littoral Opal Coast , Boulogne sur Mer </wicri:regionArea><wicri:noRegion>Boulogne sur Mer </wicri:noRegion><wicri:noRegion>Boulogne sur Mer </wicri:noRegion></affiliation></author><author><name sortKey="Viltart, Odile" sort="Viltart, Odile" uniqKey="Viltart O" first="Odile" last="Viltart">Odile Viltart</name><affiliation wicri:level="1"><nlm:affiliation>INSERM UMR-S1172, Early stages of Parkinson diseases, University Lille 1 , Lille , France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>INSERM UMR-S1172, Early stages of Parkinson diseases, University Lille 1 , Lille </wicri:regionArea><wicri:noRegion>Lille </wicri:noRegion><wicri:noRegion>Lille </wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2015">2015</date><idno type="RBID">pubmed:26042085</idno><idno type="pmid">26042085</idno><idno type="doi">10.3389/fendo.2015.00068</idno><idno type="wicri:Area/PubMed/Corpus">000352</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000352</idno><idno type="wicri:Area/PubMed/Curation">000350</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000350</idno><idno type="wicri:Area/PubMed/Checkpoint">000350</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">000350</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">The use of animal models to decipher physiological and neurobiological alterations of anorexia nervosa patients.</title><author><name sortKey="Mequinion, Mathieu" sort="Mequinion, Mathieu" uniqKey="Mequinion M" first="Mathieu" last="Méquinion">Mathieu Méquinion</name><affiliation wicri:level="1"><nlm:affiliation>INSERM UMR-S1172, Development and Plasticity of Postnatal Brain , Lille , France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>INSERM UMR-S1172, Development and Plasticity of Postnatal Brain , Lille </wicri:regionArea><wicri:noRegion>Lille </wicri:noRegion><wicri:noRegion>Lille </wicri:noRegion></affiliation></author><author><name sortKey="Chauveau, Christophe" sort="Chauveau, Christophe" uniqKey="Chauveau C" first="Christophe" last="Chauveau">Christophe Chauveau</name><affiliation wicri:level="1"><nlm:affiliation>Pathophysiology of Inflammatory Bone Diseases, EA 4490, University of the Littoral Opal Coast , Boulogne sur Mer , France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Pathophysiology of Inflammatory Bone Diseases, EA 4490, University of the Littoral Opal Coast , Boulogne sur Mer </wicri:regionArea><wicri:noRegion>Boulogne sur Mer </wicri:noRegion><wicri:noRegion>Boulogne sur Mer </wicri:noRegion></affiliation></author><author><name sortKey="Viltart, Odile" sort="Viltart, Odile" uniqKey="Viltart O" first="Odile" last="Viltart">Odile Viltart</name><affiliation wicri:level="1"><nlm:affiliation>INSERM UMR-S1172, Early stages of Parkinson diseases, University Lille 1 , Lille , France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>INSERM UMR-S1172, Early stages of Parkinson diseases, University Lille 1 , Lille </wicri:regionArea><wicri:noRegion>Lille </wicri:noRegion><wicri:noRegion>Lille </wicri:noRegion></affiliation></author></analytic><series><title level="j">Frontiers in endocrinology</title><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Extensive studies were performed to decipher the mechanisms regulating feeding due to the worldwide obesity pandemy and its complications. The data obtained might be adapted to another disorder related to alteration of food intake, the restrictive anorexia nervosa. This multifactorial disease with a complex and unknown etiology is considered as an awful eating disorder since the chronic refusal to eat leads to severe, and sometimes, irreversible complications for the whole organism, until death. There is an urgent need to better understand the different aspects of the disease to develop novel approaches complementary to the usual psychological therapies. For this purpose, the use of pertinent animal models becomes a necessity. We present here the various rodent models described in the literature that might be used to dissect central and peripheral mechanisms involved in the adaptation to deficient energy supplies and/or the maintenance of physiological alterations on the long term. Data obtained from the spontaneous or engineered genetic models permit to better apprehend the implication of one signaling system (hormone, neuropeptide, neurotransmitter) in the development of several symptoms observed in anorexia nervosa. As example, mutations in the ghrelin, serotonin, dopamine pathways lead to alterations that mimic the phenotype, but compensatory mechanisms often occur rendering necessary the use of more selective gene strategies. Until now, environmental animal models based on one or several inducing factors like diet restriction, stress, or physical activity mimicked more extensively central and peripheral alterations decribed in anorexia nervosa. They bring significant data on feeding behavior, energy expenditure, and central circuit alterations. Animal models are described and criticized on the basis of the criteria of validity for anorexia nervosa.</div></front></TEI><pubmed><MedlineCitation Status="PubMed-not-MEDLINE" Owner="NLM"><PMID Version="1">26042085</PMID><DateCreated><Year>2015</Year><Month>06</Month><Day>04</Day></DateCreated><DateCompleted><Year>2015</Year><Month>06</Month><Day>04</Day></DateCompleted><DateRevised><Year>2015</Year><Month>06</Month><Day>06</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><JournalIssue CitedMedium="Print"><Volume>6</Volume><PubDate><Year>2015</Year></PubDate></JournalIssue><Title>Frontiers in endocrinology</Title><ISOAbbreviation>Front Endocrinol (Lausanne)</ISOAbbreviation></Journal><ArticleTitle>The use of animal models to decipher physiological and neurobiological alterations of anorexia nervosa patients.</ArticleTitle><Pagination><MedlinePgn>68</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.3389/fendo.2015.00068</ELocationID><Abstract><AbstractText>Extensive studies were performed to decipher the mechanisms regulating feeding due to the worldwide obesity pandemy and its complications. The data obtained might be adapted to another disorder related to alteration of food intake, the restrictive anorexia nervosa. This multifactorial disease with a complex and unknown etiology is considered as an awful eating disorder since the chronic refusal to eat leads to severe, and sometimes, irreversible complications for the whole organism, until death. There is an urgent need to better understand the different aspects of the disease to develop novel approaches complementary to the usual psychological therapies. For this purpose, the use of pertinent animal models becomes a necessity. We present here the various rodent models described in the literature that might be used to dissect central and peripheral mechanisms involved in the adaptation to deficient energy supplies and/or the maintenance of physiological alterations on the long term. Data obtained from the spontaneous or engineered genetic models permit to better apprehend the implication of one signaling system (hormone, neuropeptide, neurotransmitter) in the development of several symptoms observed in anorexia nervosa. As example, mutations in the ghrelin, serotonin, dopamine pathways lead to alterations that mimic the phenotype, but compensatory mechanisms often occur rendering necessary the use of more selective gene strategies. Until now, environmental animal models based on one or several inducing factors like diet restriction, stress, or physical activity mimicked more extensively central and peripheral alterations decribed in anorexia nervosa. They bring significant data on feeding behavior, energy expenditure, and central circuit alterations. Animal models are described and criticized on the basis of the criteria of validity for anorexia nervosa.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Méquinion</LastName><ForeName>Mathieu</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>INSERM UMR-S1172, Development and Plasticity of Postnatal Brain , Lille , France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chauveau</LastName><ForeName>Christophe</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Pathophysiology of Inflammatory Bone Diseases, EA 4490, University of the Littoral Opal Coast , Boulogne sur Mer , France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Viltart</LastName><ForeName>Odile</ForeName><Initials>O</Initials><AffiliationInfo><Affiliation>INSERM UMR-S1172, Early stages of Parkinson diseases, University Lille 1 , Lille , France.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2015</Year><Month>05</Month><Day>19</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Front Endocrinol (Lausanne)</MedlineTA><NlmUniqueID>101555782</NlmUniqueID><ISSNLinking>1664-2392</ISSNLinking></MedlineJournalInfo><OtherID Source="NLM">PMC4436882</OtherID><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">activity/hyperactivity</Keyword><Keyword MajorTopicYN="N">acute stress</Keyword><Keyword MajorTopicYN="N">anorexia nervosa</Keyword><Keyword MajorTopicYN="N">environmental models</Keyword><Keyword MajorTopicYN="N">food restriction</Keyword><Keyword MajorTopicYN="N">genetic models</Keyword><Keyword MajorTopicYN="N">social stress</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2015</Year><Month>02</Month><Day>12</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2015</Year><Month>04</Month><Day>15</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2015</Year><Month>6</Month><Day>5</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2015</Year><Month>6</Month><Day>5</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2015</Year><Month>6</Month><Day>5</Day><Hour>6</Hour><Minute>1</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">26042085</ArticleId><ArticleId IdType="doi">10.3389/fendo.2015.00068</ArticleId><ArticleId IdType="pmc">PMC4436882</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>France</li></country></list><tree><country name="France"><noRegion><name sortKey="Mequinion, Mathieu" sort="Mequinion, Mathieu" uniqKey="Mequinion M" first="Mathieu" last="Méquinion">Mathieu Méquinion</name></noRegion><name sortKey="Chauveau, Christophe" sort="Chauveau, Christophe" uniqKey="Chauveau C" first="Christophe" last="Chauveau">Christophe Chauveau</name><name sortKey="Viltart, Odile" sort="Viltart, Odile" uniqKey="Viltart O" first="Odile" last="Viltart">Odile Viltart</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/ParkinsonFranceV1/Data/PubMed/Checkpoint
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000252 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/PubMed/Checkpoint/biblio.hfd -nk 000252 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Sante
|area= ParkinsonFranceV1
|flux= PubMed
|étape= Checkpoint
|type= RBID
|clé= pubmed:26042085
|texte= The use of animal models to decipher physiological and neurobiological alterations of anorexia nervosa patients.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/PubMed/Checkpoint/RBID.i -Sk "pubmed:26042085" \
| HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Checkpoint/biblio.hfd \
| NlmPubMed2Wicri -a ParkinsonFranceV1
| This area was generated with Dilib version V0.6.29. |  |