Effects of subthalamic nucleus deep brain stimulation and levodopa on energy production rate and substrate oxidation in Parkinson's disease.
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/l; 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.
Perlemoine
Caroline
C
Service de Neurologie, Hôpital Haut-Lévêque, Pessac, France. caroline.perlemoine@chu-bordeaux.fr
Macia
Frédéric
F
Tison
François
F
Coman
Isabelle
I
Guehl
Dominique
D
Burbaud
Pierre
P
Cuny
Emmanuel
E
Baillet
Laurence
L
Gin
Henri
H
Rigalleau
Vincent
V
D000978:Antiparkinson Agents / Q000627:therapeutic use*; D001786:Blood Glucose / Q000378:metabolism; D001798:Blood Proteins / Q000378:metabolism; D004558:Electric Stimulation / Q000379:methods; D002149:Energy Intake / Q000502:physiology; D004734:Energy Metabolism / Q000187:drug effects / Q000502:physiology*; D005215:Fasting / Q000502:physiology; D005260:Female; D005947:Glucose / Q000378:metabolism; D006801:Humans; D007980:Levodopa / Q000627:therapeutic use*; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D010084:Oxidation-Reduction / Q000187:drug effects; D010300:Parkinson Disease / Q000188:drug therapy / Q000503:physiopathology*; D020531:Subthalamic Nucleus / Q000503:physiopathology*; D015430:Weight Gain / Q000187:drug effects / Q000502:physiology
D000978:Antiparkinson Agents; D001786:Blood Glucose; D001798:Blood Proteins; D008055:Lipids; D007980:Levodopa; D005947:Glucose