Mechanisms of body weight gain in patients with Parkinson's disease after subthalamic stimulation.
Identifieur interne : 000D71 ( PubMed/Corpus ); précédent : 000D70; suivant : 000D72Mechanisms of body weight gain in patients with Parkinson's disease after subthalamic stimulation.
Auteurs : C. Montaurier ; B. Morio ; S. Bannier ; P. Derost ; P. Arnaud ; M. Brandolini-Bunlon ; C. Giraudet ; Y. Boirie ; F. DurifSource :
- Brain : a journal of neurology [ 1460-2156 ] ; 2007.
English descriptors
- KwdEn :
- Antiparkinson Agents (therapeutic use), Basal Metabolism, Body Composition, Calorimetry, Indirect (methods), Deep Brain Stimulation, Eating, Electrodes, Implanted, Energy Intake, Energy Metabolism, Female, Humans, Levodopa (therapeutic use), Male, Middle Aged, Parkinson Disease (drug therapy), Parkinson Disease (physiopathology), Parkinson Disease (therapy), Prospective Studies, Stereotaxic Techniques, Subthalamic Nucleus (physiopathology), Treatment Outcome, Weight Gain.
- MESH :
- chemical , therapeutic use : Antiparkinson Agents, Levodopa.
- drug therapy : Parkinson Disease.
- methods : Calorimetry, Indirect.
- physiopathology : Parkinson Disease, Subthalamic Nucleus.
- therapy : Parkinson Disease.
- Basal Metabolism, Body Composition, Deep Brain Stimulation, Eating, Electrodes, Implanted, Energy Intake, Energy Metabolism, Female, Humans, Male, Middle Aged, Prospective Studies, Stereotaxic Techniques, Treatment Outcome, Weight Gain.
Abstract
Chronic bilateral subthalamic stimulation leads to a spectacular clinical improvement in patients with motor complications. However, the post-operative body weight gain involved may limit the benefits of surgery and induce critical metabolic disorders. Twenty-four Parkinsonians (61.1 +/- 1.4 years) were examined 1 month before (M - 1) and 3 months after (M + 3) surgery. Body composition and energy expenditure (EE) were measured (1) over 36 h in calorimetric chambers (CC) with rigorous control of food intakes and activities [sleep metabolic rate, resting activities, meals, 3 or 4 sessions of 20 min on a training bicycle at 13 km/h and daily EE] and (2) in resting conditions (basal metabolic rate) during an acute L-dopa challenge (M - 1) or according to acute 'off' and 'on' stimulation (M + 3). Before surgery, EE was compared between the Parkinsonian patients and healthy subjects matched for height and body composition (metabolic rate during sleep, daily EE) or matched to predicted values (basal metabolic rate). Before surgery, in Parkinsonian men but not women, (1) daily EE was higher while sleep metabolic rate was lower compared to healthy matched men (+9.2 +/- 3.9 and -8.2 +/- 2.3%, respectively, P < 0.05) and (2) basal metabolic rate (L-dopa 'on') was higher than predicted basal metabolic rate (+11.5 +/- 4.0%, P < 0.05) but was further increased without L-dopa (+8.4 +/- 3.2% vs L-dopa 'on', P < 0.05). EE during daily activities was higher during 'off' periods compared to 'on' periods for both men (+19.3 +/- 3.3%, P < 0.0001) and women (+16.1 +/- 4.7%, P < 0.01). After surgery, there was a 3.4 +/- 0.6 kg (P < 0.0001) body weight increase together with fat mass (P < 0.0001) and fat-free mass (P < 0.05) in Parkinsonian men and a 2.6 +/- 0.8 kg (P < 0.05) body weight increase together with fat mass (P < 0.05) in Parkinsonian women. Sleep metabolic rate increased in men (+7.5 +/- 2.0%, P < 0.01) to reach control values but remained unchanged in women. Daily EE decreased significantly in both men and women (-7.3 +/- 2.2% and -13.1 +/- 1.7%, respectively, P < 0.01) but there was no correlation between daily EE changes and body weight gain. Parkinson's disease is associated with profound alterations in the central control of energy metabolism. Normalization of energy metabolism after DBS-STN implantation may favour body weight gain, of which quality was gender specific. As men gained primarily fat-free mass, a reasonable weight gain may be tolerated, in contrast with women who gained only fat. Other factors such as changes in free-living physical activity may help to limit body weight gain in some patients.
DOI: 10.1093/brain/awm113
PubMed: 17535833
Links to Exploration step
pubmed:17535833Le document en format XML
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Arnaud</name></author><author><name sortKey="Brandolini Bunlon, M" sort="Brandolini Bunlon, M" uniqKey="Brandolini Bunlon M" first="M" last="Brandolini-Bunlon">M. Brandolini-Bunlon</name></author><author><name sortKey="Giraudet, C" sort="Giraudet, C" uniqKey="Giraudet C" first="C" last="Giraudet">C. Giraudet</name></author><author><name sortKey="Boirie, Y" sort="Boirie, Y" uniqKey="Boirie Y" first="Y" last="Boirie">Y. Boirie</name></author><author><name sortKey="Durif, F" sort="Durif, F" uniqKey="Durif F" first="F" last="Durif">F. Durif</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2007">2007</date><idno type="RBID">pubmed:17535833</idno><idno type="pmid">17535833</idno><idno type="doi">10.1093/brain/awm113</idno><idno type="wicri:Area/PubMed/Corpus">000D71</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000D71</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Mechanisms of body weight gain in patients with Parkinson's disease after subthalamic stimulation.</title><author><name sortKey="Montaurier, C" sort="Montaurier, C" uniqKey="Montaurier C" first="C" last="Montaurier">C. Montaurier</name><affiliation><nlm:affiliation>INRA, Centre Clermont-Ferrand-Theix, UMR 1019, Unité de Nutrition Humaine, CRNH Auvergne, Clermont-Ferrand, F-63009 France.</nlm:affiliation></affiliation></author><author><name sortKey="Morio, B" sort="Morio, B" uniqKey="Morio B" first="B" last="Morio">B. Morio</name></author><author><name sortKey="Bannier, S" sort="Bannier, S" uniqKey="Bannier S" first="S" last="Bannier">S. Bannier</name></author><author><name sortKey="Derost, P" sort="Derost, P" uniqKey="Derost P" first="P" last="Derost">P. Derost</name></author><author><name sortKey="Arnaud, P" sort="Arnaud, P" uniqKey="Arnaud P" first="P" last="Arnaud">P. Arnaud</name></author><author><name sortKey="Brandolini Bunlon, M" sort="Brandolini Bunlon, M" uniqKey="Brandolini Bunlon M" first="M" last="Brandolini-Bunlon">M. Brandolini-Bunlon</name></author><author><name sortKey="Giraudet, C" sort="Giraudet, C" uniqKey="Giraudet C" first="C" last="Giraudet">C. Giraudet</name></author><author><name sortKey="Boirie, Y" sort="Boirie, Y" uniqKey="Boirie Y" first="Y" last="Boirie">Y. Boirie</name></author><author><name sortKey="Durif, F" sort="Durif, F" uniqKey="Durif F" first="F" last="Durif">F. Durif</name></author></analytic><series><title level="j">Brain : a journal of neurology</title><idno type="eISSN">1460-2156</idno><imprint><date when="2007" type="published">2007</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antiparkinson Agents (therapeutic use)</term><term>Basal Metabolism</term><term>Body Composition</term><term>Calorimetry, Indirect (methods)</term><term>Deep Brain Stimulation</term><term>Eating</term><term>Electrodes, Implanted</term><term>Energy Intake</term><term>Energy Metabolism</term><term>Female</term><term>Humans</term><term>Levodopa (therapeutic use)</term><term>Male</term><term>Middle Aged</term><term>Parkinson Disease (drug therapy)</term><term>Parkinson Disease (physiopathology)</term><term>Parkinson Disease (therapy)</term><term>Prospective Studies</term><term>Stereotaxic Techniques</term><term>Subthalamic Nucleus (physiopathology)</term><term>Treatment Outcome</term><term>Weight Gain</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Calorimetry, Indirect</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Parkinson Disease</term><term>Subthalamic Nucleus</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Basal Metabolism</term><term>Body Composition</term><term>Deep Brain Stimulation</term><term>Eating</term><term>Electrodes, Implanted</term><term>Energy Intake</term><term>Energy Metabolism</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Prospective Studies</term><term>Stereotaxic Techniques</term><term>Treatment Outcome</term><term>Weight Gain</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Chronic bilateral subthalamic stimulation leads to a spectacular clinical improvement in patients with motor complications. However, the post-operative body weight gain involved may limit the benefits of surgery and induce critical metabolic disorders. Twenty-four Parkinsonians (61.1 +/- 1.4 years) were examined 1 month before (M - 1) and 3 months after (M + 3) surgery. Body composition and energy expenditure (EE) were measured (1) over 36 h in calorimetric chambers (CC) with rigorous control of food intakes and activities [sleep metabolic rate, resting activities, meals, 3 or 4 sessions of 20 min on a training bicycle at 13 km/h and daily EE] and (2) in resting conditions (basal metabolic rate) during an acute L-dopa challenge (M - 1) or according to acute 'off' and 'on' stimulation (M + 3). Before surgery, EE was compared between the Parkinsonian patients and healthy subjects matched for height and body composition (metabolic rate during sleep, daily EE) or matched to predicted values (basal metabolic rate). Before surgery, in Parkinsonian men but not women, (1) daily EE was higher while sleep metabolic rate was lower compared to healthy matched men (+9.2 +/- 3.9 and -8.2 +/- 2.3%, respectively, P < 0.05) and (2) basal metabolic rate (L-dopa 'on') was higher than predicted basal metabolic rate (+11.5 +/- 4.0%, P < 0.05) but was further increased without L-dopa (+8.4 +/- 3.2% vs L-dopa 'on', P < 0.05). EE during daily activities was higher during 'off' periods compared to 'on' periods for both men (+19.3 +/- 3.3%, P < 0.0001) and women (+16.1 +/- 4.7%, P < 0.01). After surgery, there was a 3.4 +/- 0.6 kg (P < 0.0001) body weight increase together with fat mass (P < 0.0001) and fat-free mass (P < 0.05) in Parkinsonian men and a 2.6 +/- 0.8 kg (P < 0.05) body weight increase together with fat mass (P < 0.05) in Parkinsonian women. Sleep metabolic rate increased in men (+7.5 +/- 2.0%, P < 0.01) to reach control values but remained unchanged in women. Daily EE decreased significantly in both men and women (-7.3 +/- 2.2% and -13.1 +/- 1.7%, respectively, P < 0.01) but there was no correlation between daily EE changes and body weight gain. Parkinson's disease is associated with profound alterations in the central control of energy metabolism. Normalization of energy metabolism after DBS-STN implantation may favour body weight gain, of which quality was gender specific. As men gained primarily fat-free mass, a reasonable weight gain may be tolerated, in contrast with women who gained only fat. Other factors such as changes in free-living physical activity may help to limit body weight gain in some patients.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">17535833</PMID><DateCreated><Year>2007</Year><Month>06</Month><Day>22</Day></DateCreated><DateCompleted><Year>2007</Year><Month>07</Month><Day>24</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1460-2156</ISSN><JournalIssue CitedMedium="Internet"><Volume>130</Volume><Issue>Pt 7</Issue><PubDate><Year>2007</Year><Month>Jul</Month></PubDate></JournalIssue><Title>Brain : a journal of neurology</Title><ISOAbbreviation>Brain</ISOAbbreviation></Journal><ArticleTitle>Mechanisms of body weight gain in patients with Parkinson's disease after subthalamic stimulation.</ArticleTitle><Pagination><MedlinePgn>1808-18</MedlinePgn></Pagination><Abstract><AbstractText>Chronic bilateral subthalamic stimulation leads to a spectacular clinical improvement in patients with motor complications. However, the post-operative body weight gain involved may limit the benefits of surgery and induce critical metabolic disorders. Twenty-four Parkinsonians (61.1 +/- 1.4 years) were examined 1 month before (M - 1) and 3 months after (M + 3) surgery. Body composition and energy expenditure (EE) were measured (1) over 36 h in calorimetric chambers (CC) with rigorous control of food intakes and activities [sleep metabolic rate, resting activities, meals, 3 or 4 sessions of 20 min on a training bicycle at 13 km/h and daily EE] and (2) in resting conditions (basal metabolic rate) during an acute L-dopa challenge (M - 1) or according to acute 'off' and 'on' stimulation (M + 3). Before surgery, EE was compared between the Parkinsonian patients and healthy subjects matched for height and body composition (metabolic rate during sleep, daily EE) or matched to predicted values (basal metabolic rate). Before surgery, in Parkinsonian men but not women, (1) daily EE was higher while sleep metabolic rate was lower compared to healthy matched men (+9.2 +/- 3.9 and -8.2 +/- 2.3%, respectively, P < 0.05) and (2) basal metabolic rate (L-dopa 'on') was higher than predicted basal metabolic rate (+11.5 +/- 4.0%, P < 0.05) but was further increased without L-dopa (+8.4 +/- 3.2% vs L-dopa 'on', P < 0.05). EE during daily activities was higher during 'off' periods compared to 'on' periods for both men (+19.3 +/- 3.3%, P < 0.0001) and women (+16.1 +/- 4.7%, P < 0.01). After surgery, there was a 3.4 +/- 0.6 kg (P < 0.0001) body weight increase together with fat mass (P < 0.0001) and fat-free mass (P < 0.05) in Parkinsonian men and a 2.6 +/- 0.8 kg (P < 0.05) body weight increase together with fat mass (P < 0.05) in Parkinsonian women. Sleep metabolic rate increased in men (+7.5 +/- 2.0%, P < 0.01) to reach control values but remained unchanged in women. Daily EE decreased significantly in both men and women (-7.3 +/- 2.2% and -13.1 +/- 1.7%, respectively, P < 0.01) but there was no correlation between daily EE changes and body weight gain. Parkinson's disease is associated with profound alterations in the central control of energy metabolism. Normalization of energy metabolism after DBS-STN implantation may favour body weight gain, of which quality was gender specific. As men gained primarily fat-free mass, a reasonable weight gain may be tolerated, in contrast with women who gained only fat. Other factors such as changes in free-living physical activity may help to limit body weight gain in some patients.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Montaurier</LastName><ForeName>C</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>INRA, Centre Clermont-Ferrand-Theix, UMR 1019, Unité de Nutrition Humaine, CRNH Auvergne, Clermont-Ferrand, F-63009 France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Morio</LastName><ForeName>B</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Bannier</LastName><ForeName>S</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Derost</LastName><ForeName>P</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Arnaud</LastName><ForeName>P</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Brandolini-Bunlon</LastName><ForeName>M</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Giraudet</LastName><ForeName>C</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Boirie</LastName><ForeName>Y</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Durif</LastName><ForeName>F</ForeName><Initials>F</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2007</Year><Month>05</Month><Day>29</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Brain</MedlineTA><NlmUniqueID>0372537</NlmUniqueID><ISSNLinking>0006-8950</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000978">Antiparkinson Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>46627O600J</RegistryNumber><NameOfSubstance UI="D007980">Levodopa</NameOfSubstance></Chemical></ChemicalList><CitationSubset>AIM</CitationSubset><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000978" MajorTopicYN="N">Antiparkinson Agents</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001481" MajorTopicYN="N">Basal Metabolism</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001823" MajorTopicYN="N">Body Composition</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002153" MajorTopicYN="N">Calorimetry, Indirect</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D046690" MajorTopicYN="Y">Deep Brain Stimulation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004435" MajorTopicYN="N">Eating</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004567" MajorTopicYN="N">Electrodes, Implanted</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002149" MajorTopicYN="N">Energy Intake</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004734" MajorTopicYN="N">Energy Metabolism</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007980" MajorTopicYN="N">Levodopa</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName><QualifierName UI="Q000628" MajorTopicYN="Y">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011446" MajorTopicYN="N">Prospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013238" MajorTopicYN="N">Stereotaxic Techniques</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020531" MajorTopicYN="N">Subthalamic Nucleus</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016896" MajorTopicYN="N">Treatment Outcome</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015430" MajorTopicYN="Y">Weight Gain</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2007</Year><Month>5</Month><Day>31</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2007</Year><Month>7</Month><Day>25</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2007</Year><Month>5</Month><Day>31</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">17535833</ArticleId><ArticleId IdType="pii">awm113</ArticleId><ArticleId IdType="doi">10.1093/brain/awm113</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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