Effects of subthalamic nucleus deep brain stimulation and levodopa on energy production rate and substrate oxidation in parkinson's disease
Identifieur interne : 000C19 ( PascalFrancis/Corpus ); précédent : 000C18; suivant : 000C20Effects of subthalamic nucleus deep brain stimulation and levodopa on energy production rate and substrate oxidation in parkinson's disease
Auteurs : Caroline Perlemoine ; Frédéric Macia ; Francois Tison ; Isabelle Coman ; Dominique Guehl ; Pierre Burbaud ; Emmanuel Cuny ; Laurence Baillet ; Henri Gins ; Vincent RigalleauSource :
- British Journal of Nutrition [ 0007-1145 ] ; 2005.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
Abstract
Patients with Parkinson's disease (PD) often lose weight, but after subthalamic nucleus deep brain stimulation (STN-DBS), they gain weight. We compared daily energy intake (DEI), resting energy expenditure (REE) and substrate oxidation rates (measured by indirect calorimetry) in nineteen STN-DBS-treated patients (Group S), thirteen others on pharmacologic treatment by levodopa (Group L) and eight control subjects. We also determined the acute effects of STN-DBS and levodopa on REE and substrate oxidation rates. STN-DBS treated patients gained 9.7 (SEM 7.1) kg after surgery, whereas patients on pharmacologic treatment lost 3.8 (SEM 10.0) kg since diagnosis. In STN-DBS-treated patients, REE (-16.5%; P<0.001), lipid oxidation (-27%; P<0.05) and protein oxidation (-46 %; P<0.05) were decreased, whereas glucose oxidation was elevated (+81 %; P<0.05) as compared to patients on pharmacologic treatment. Levodopa acutely reduced REE (-8.3%; P<0.05) and glucose oxidation (-37 %; P<0.01) with a slight hyperglycaemic effect (after levodopa challenge: 5.6 (SEM 0.8) v. before levodopa challenge: 5.3 (SEM 0.6) mmol/l; P<0.01). Switching 'on' STN-DBS acutely reduced REE (- 17.5%; P<0.01) and lipid oxidation (-24%; P<0◦.001) 30 min after starting stimulation. Fasting glycaemia was slightly but significantly reduced (5.4 (SEM 1-4) v. 5.5 (SEM 1.3) mmol/1; P<0.01). After STN-DBS, the normalization of REE and the reduction in lipid and protein oxidation contribute to the restoration of weight. As levodopa decreases glucose oxidation, the reduction in daily dose of levodopa in STN-DBS-treated patients helps prevent the effect of weight gain on glycaemia.
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Format Inist (serveur)
NO : | PASCAL 06-0038622 INIST |
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ET : | Effects of subthalamic nucleus deep brain stimulation and levodopa on energy production rate and substrate oxidation in parkinson's disease |
AU : | PERLEMOINE (Caroline); MACIA (Frédéric); TISON (Francois); COMAN (Isabelle); GUEHL (Dominique); BURBAUD (Pierre); CUNY (Emmanuel); BAILLET (Laurence); GINS (Henri); RIGALLEAU (Vincent) |
AF : | Service de Nutrition-Diabétologie, Hôpital Haut-Lévêque, Avenue Magellan/33600 Pessac/France (1 aut., 8 aut., 9 aut., 10 aut.); Service de Neurologie, Hôpital Haut-Lévêque/Pessac/France (2 aut., 3 aut., 4 aut., 5 aut., 6 aut.); Service de Neurochirurgie, Hôpital du Tripode/Bordeaux/France (7 aut.) |
DT : | Publication en série; Niveau analytique |
SO : | British Journal of Nutrition; ISSN 0007-1145; Royaume-Uni; Da. 2005; Vol. 93; No. 2; Pp. 191-198; Bibl. 31 ref. |
LA : | Anglais |
EA : | Patients with Parkinson's disease (PD) often lose weight, but after subthalamic nucleus deep brain stimulation (STN-DBS), they gain weight. We compared daily energy intake (DEI), resting energy expenditure (REE) and substrate oxidation rates (measured by indirect calorimetry) in nineteen STN-DBS-treated patients (Group S), thirteen others on pharmacologic treatment by levodopa (Group L) and eight control subjects. We also determined the acute effects of STN-DBS and levodopa on REE and substrate oxidation rates. STN-DBS treated patients gained 9.7 (SEM 7.1) kg after surgery, whereas patients on pharmacologic treatment lost 3.8 (SEM 10.0) kg since diagnosis. In STN-DBS-treated patients, REE (-16.5%; P<0.001), lipid oxidation (-27%; P<0.05) and protein oxidation (-46 %; P<0.05) were decreased, whereas glucose oxidation was elevated (+81 %; P<0.05) as compared to patients on pharmacologic treatment. Levodopa acutely reduced REE (-8.3%; P<0.05) and glucose oxidation (-37 %; P<0.01) with a slight hyperglycaemic effect (after levodopa challenge: 5.6 (SEM 0.8) v. before levodopa challenge: 5.3 (SEM 0.6) mmol/l; P<0.01). Switching 'on' STN-DBS acutely reduced REE (- 17.5%; P<0.01) and lipid oxidation (-24%; P<0◦.001) 30 min after starting stimulation. Fasting glycaemia was slightly but significantly reduced (5.4 (SEM 1-4) v. 5.5 (SEM 1.3) mmol/1; P<0.01). After STN-DBS, the normalization of REE and the reduction in lipid and protein oxidation contribute to the restoration of weight. As levodopa decreases glucose oxidation, the reduction in daily dose of levodopa in STN-DBS-treated patients helps prevent the effect of weight gain on glycaemia. |
CC : | 002A16E |
FD : | Noyau sousthalamique; Energie; Taux production; Substrat; Oxydation; Dépense énergétique; Poids; Changement; Parkinson maladie; Régime alimentaire; Thermogenèse; Mammalia |
FG : | Vertebrata; Encéphale pathologie; Système nerveux central; Extrapyramidal syndrome; Maladie dégénérative; Système nerveux central pathologie; Système nerveux pathologie; Alimentation |
ED : | Subthalamic nucleus; Energy; Production rate; Substrate; Oxidation; Energetic cost; Weight; Change; Parkinson disease; Diet; Thermogenesis; Mammalia |
EG : | Vertebrata; Cerebral disorder; Central nervous system; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease; Nervous system diseases; Feeding |
SD : | Núcleo subtalámico; Energía; Índice producción; Substrato; Oxidación; Costo energético; Peso; Cambio; Parkinson enfermedad; Régimen alimentario; Termogénesis; Mammalia |
LO : | INIST-2404.354000125987450050 |
ID : | 06-0038622 |
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Pascal:06-0038622Le document en format XML
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<series><title level="j" type="main">British Journal of Nutrition</title>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Change</term>
<term>Diet</term>
<term>Energetic cost</term>
<term>Energy</term>
<term>Mammalia</term>
<term>Oxidation</term>
<term>Parkinson disease</term>
<term>Production rate</term>
<term>Substrate</term>
<term>Subthalamic nucleus</term>
<term>Thermogenesis</term>
<term>Weight</term>
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<term>Oxydation</term>
<term>Dépense énergétique</term>
<term>Poids</term>
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<front><div type="abstract" xml:lang="en">Patients with Parkinson's disease (PD) often lose weight, but after subthalamic nucleus deep brain stimulation (STN-DBS), they gain weight. We compared daily energy intake (DEI), resting energy expenditure (REE) and substrate oxidation rates (measured by indirect calorimetry) in nineteen STN-DBS-treated patients (Group S), thirteen others on pharmacologic treatment by levodopa (Group L) and eight control subjects. We also determined the acute effects of STN-DBS and levodopa on REE and substrate oxidation rates. STN-DBS treated patients gained 9.7 (SEM 7.1) kg after surgery, whereas patients on pharmacologic treatment lost 3.8 (SEM 10.0) kg since diagnosis. In STN-DBS-treated patients, REE (-16.5%; P<0.001), lipid oxidation (-27%; P<0.05) and protein oxidation (-46 %; P<0.05) were decreased, whereas glucose oxidation was elevated (+81 %; P<0.05) as compared to patients on pharmacologic treatment. Levodopa acutely reduced REE (-8.3%; P<0.05) and glucose oxidation (-37 %; P<0.01) with a slight hyperglycaemic effect (after levodopa challenge: 5.6 (SEM 0.8) v. before levodopa challenge: 5.3 (SEM 0.6) mmol/l; P<0.01). Switching 'on' STN-DBS acutely reduced REE (- 17.5%; P<0.01) and lipid oxidation (-24%; P<0◦.001) 30 min after starting stimulation. Fasting glycaemia was slightly but significantly reduced (5.4 (SEM 1-4) v. 5.5 (SEM 1.3) mmol/1; P<0.01). After STN-DBS, the normalization of REE and the reduction in lipid and protein oxidation contribute to the restoration of weight. As levodopa decreases glucose oxidation, the reduction in daily dose of levodopa in STN-DBS-treated patients helps prevent the effect of weight gain on glycaemia.</div>
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<fC01 i1="01" l="ENG"><s0>Patients with Parkinson's disease (PD) often lose weight, but after subthalamic nucleus deep brain stimulation (STN-DBS), they gain weight. We compared daily energy intake (DEI), resting energy expenditure (REE) and substrate oxidation rates (measured by indirect calorimetry) in nineteen STN-DBS-treated patients (Group S), thirteen others on pharmacologic treatment by levodopa (Group L) and eight control subjects. We also determined the acute effects of STN-DBS and levodopa on REE and substrate oxidation rates. STN-DBS treated patients gained 9.7 (SEM 7.1) kg after surgery, whereas patients on pharmacologic treatment lost 3.8 (SEM 10.0) kg since diagnosis. In STN-DBS-treated patients, REE (-16.5%; P<0.001), lipid oxidation (-27%; P<0.05) and protein oxidation (-46 %; P<0.05) were decreased, whereas glucose oxidation was elevated (+81 %; P<0.05) as compared to patients on pharmacologic treatment. Levodopa acutely reduced REE (-8.3%; P<0.05) and glucose oxidation (-37 %; P<0.01) with a slight hyperglycaemic effect (after levodopa challenge: 5.6 (SEM 0.8) v. before levodopa challenge: 5.3 (SEM 0.6) mmol/l; P<0.01). Switching 'on' STN-DBS acutely reduced REE (- 17.5%; P<0.01) and lipid oxidation (-24%; P<0◦.001) 30 min after starting stimulation. Fasting glycaemia was slightly but significantly reduced (5.4 (SEM 1-4) v. 5.5 (SEM 1.3) mmol/1; P<0.01). After STN-DBS, the normalization of REE and the reduction in lipid and protein oxidation contribute to the restoration of weight. As levodopa decreases glucose oxidation, the reduction in daily dose of levodopa in STN-DBS-treated patients helps prevent the effect of weight gain on glycaemia.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002A16E</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Noyau sousthalamique</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Subthalamic nucleus</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Núcleo subtalámico</s0>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Energie</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Energy</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Energía</s0>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Taux production</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Production rate</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Índice producción</s0>
<s5>03</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Substrat</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Substrate</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Substrato</s0>
<s5>04</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Oxydation</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Oxidation</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Oxidación</s0>
<s5>05</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Dépense énergétique</s0>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Energetic cost</s0>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Costo energético</s0>
<s5>06</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Poids</s0>
<s5>07</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Weight</s0>
<s5>07</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Peso</s0>
<s5>07</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Changement</s0>
<s5>08</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Change</s0>
<s5>08</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Cambio</s0>
<s5>08</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE"><s0>Parkinson maladie</s0>
<s5>09</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG"><s0>Parkinson disease</s0>
<s5>09</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA"><s0>Parkinson enfermedad</s0>
<s5>09</s5>
</fC03>
<fC03 i1="10" i2="X" l="FRE"><s0>Régime alimentaire</s0>
<s5>10</s5>
</fC03>
<fC03 i1="10" i2="X" l="ENG"><s0>Diet</s0>
<s5>10</s5>
</fC03>
<fC03 i1="10" i2="X" l="SPA"><s0>Régimen alimentario</s0>
<s5>10</s5>
</fC03>
<fC03 i1="11" i2="X" l="FRE"><s0>Thermogenèse</s0>
<s5>11</s5>
</fC03>
<fC03 i1="11" i2="X" l="ENG"><s0>Thermogenesis</s0>
<s5>11</s5>
</fC03>
<fC03 i1="11" i2="X" l="SPA"><s0>Termogénesis</s0>
<s5>11</s5>
</fC03>
<fC03 i1="12" i2="X" l="FRE"><s0>Mammalia</s0>
<s2>NS</s2>
<s5>13</s5>
</fC03>
<fC03 i1="12" i2="X" l="ENG"><s0>Mammalia</s0>
<s2>NS</s2>
<s5>13</s5>
</fC03>
<fC03 i1="12" i2="X" l="SPA"><s0>Mammalia</s0>
<s2>NS</s2>
<s5>13</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Encéphale pathologie</s0>
<s5>20</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>20</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>20</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Système nerveux central</s0>
<s5>21</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Central nervous system</s0>
<s5>21</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Sistema nervioso central</s0>
<s5>21</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Extrapyramidal syndrome</s0>
<s5>22</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0>
<s5>22</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0>
<s5>22</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Maladie dégénérative</s0>
<s5>23</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Degenerative disease</s0>
<s5>23</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>23</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Système nerveux central pathologie</s0>
<s5>24</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Central nervous system disease</s0>
<s5>24</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0>
<s5>24</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Système nerveux pathologie</s0>
<s5>25</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Nervous system diseases</s0>
<s5>25</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Sistema nervioso patología</s0>
<s5>25</s5>
</fC07>
<fC07 i1="08" i2="X" l="FRE"><s0>Alimentation</s0>
<s5>26</s5>
</fC07>
<fC07 i1="08" i2="X" l="ENG"><s0>Feeding</s0>
<s5>26</s5>
</fC07>
<fC07 i1="08" i2="X" l="SPA"><s0>Alimentación</s0>
<s5>26</s5>
</fC07>
<fN21><s1>016</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
</standard>
<server><NO>PASCAL 06-0038622 INIST</NO>
<ET>Effects of subthalamic nucleus deep brain stimulation and levodopa on energy production rate and substrate oxidation in parkinson's disease</ET>
<AU>PERLEMOINE (Caroline); MACIA (Frédéric); TISON (Francois); COMAN (Isabelle); GUEHL (Dominique); BURBAUD (Pierre); CUNY (Emmanuel); BAILLET (Laurence); GINS (Henri); RIGALLEAU (Vincent)</AU>
<AF>Service de Nutrition-Diabétologie, Hôpital Haut-Lévêque, Avenue Magellan/33600 Pessac/France (1 aut., 8 aut., 9 aut., 10 aut.); Service de Neurologie, Hôpital Haut-Lévêque/Pessac/France (2 aut., 3 aut., 4 aut., 5 aut., 6 aut.); Service de Neurochirurgie, Hôpital du Tripode/Bordeaux/France (7 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>British Journal of Nutrition; ISSN 0007-1145; Royaume-Uni; Da. 2005; Vol. 93; No. 2; Pp. 191-198; Bibl. 31 ref.</SO>
<LA>Anglais</LA>
<EA>Patients with Parkinson's disease (PD) often lose weight, but after subthalamic nucleus deep brain stimulation (STN-DBS), they gain weight. We compared daily energy intake (DEI), resting energy expenditure (REE) and substrate oxidation rates (measured by indirect calorimetry) in nineteen STN-DBS-treated patients (Group S), thirteen others on pharmacologic treatment by levodopa (Group L) and eight control subjects. We also determined the acute effects of STN-DBS and levodopa on REE and substrate oxidation rates. STN-DBS treated patients gained 9.7 (SEM 7.1) kg after surgery, whereas patients on pharmacologic treatment lost 3.8 (SEM 10.0) kg since diagnosis. In STN-DBS-treated patients, REE (-16.5%; P<0.001), lipid oxidation (-27%; P<0.05) and protein oxidation (-46 %; P<0.05) were decreased, whereas glucose oxidation was elevated (+81 %; P<0.05) as compared to patients on pharmacologic treatment. Levodopa acutely reduced REE (-8.3%; P<0.05) and glucose oxidation (-37 %; P<0.01) with a slight hyperglycaemic effect (after levodopa challenge: 5.6 (SEM 0.8) v. before levodopa challenge: 5.3 (SEM 0.6) mmol/l; P<0.01). Switching 'on' STN-DBS acutely reduced REE (- 17.5%; P<0.01) and lipid oxidation (-24%; P<0◦.001) 30 min after starting stimulation. Fasting glycaemia was slightly but significantly reduced (5.4 (SEM 1-4) v. 5.5 (SEM 1.3) mmol/1; P<0.01). After STN-DBS, the normalization of REE and the reduction in lipid and protein oxidation contribute to the restoration of weight. As levodopa decreases glucose oxidation, the reduction in daily dose of levodopa in STN-DBS-treated patients helps prevent the effect of weight gain on glycaemia.</EA>
<CC>002A16E</CC>
<FD>Noyau sousthalamique; Energie; Taux production; Substrat; Oxydation; Dépense énergétique; Poids; Changement; Parkinson maladie; Régime alimentaire; Thermogenèse; Mammalia</FD>
<FG>Vertebrata; Encéphale pathologie; Système nerveux central; Extrapyramidal syndrome; Maladie dégénérative; Système nerveux central pathologie; Système nerveux pathologie; Alimentation</FG>
<ED>Subthalamic nucleus; Energy; Production rate; Substrate; Oxidation; Energetic cost; Weight; Change; Parkinson disease; Diet; Thermogenesis; Mammalia</ED>
<EG>Vertebrata; Cerebral disorder; Central nervous system; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease; Nervous system diseases; Feeding</EG>
<SD>Núcleo subtalámico; Energía; Índice producción; Substrato; Oxidación; Costo energético; Peso; Cambio; Parkinson enfermedad; Régimen alimentario; Termogénesis; Mammalia</SD>
<LO>INIST-2404.354000125987450050</LO>
<ID>06-0038622</ID>
</server>
</inist>
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