Impact of Deep Brain Stimulation of Subthalamic Nucleus on the Hepatic Glucose Production in Parkinson's Disease
Parkinson' disease is a neurodegenerative disorder characterised by bradykinesia, rigidity, rest tremor and postural instability. Dopaminergic therapy such as L-Dopa and dopamine agonists usually leads to a dramatic improvement of symptoms, but disease progression nevertheless remains inevitable. Bilateral Deep brain stimulation in subthalamic nucleus (STN) leads to a spectacular clinical improvement in patients with motor complications and is now considered as the gold standard surgical treatment.
However, this surgery induces a post-operative body weight gain which may limit the benefits of this technique and induce critical metabolic disorders such as profound alterations in the central control of energy metabolism. Previous data seems to show that glucose metabolism is also altered.
The aim of this prospective study was to identify if the STN stimulation could modify glucose metabolism regulation especially the endogen glucose production (by liver) Hypothalamus is able to detect glucose concentration variations and to control/adjust glucose levels by modulating the hepatic glucose production. As hypothamus and STN are anatomically closed, we hypothesise that the STN stimulation could modulate the hypothalamus function and consequently modify glucose production.
|Idiopathic Parkinson's Disease||Behavioral: e.g., Protein and calorie controlled diet; Self-hypnotic relaxation|
|Study Design:||Allocation: Non-Randomized
Intervention Model: Crossover Assignment
Masking: Open Label
Primary Purpose: Diagnostic
|Official Title:||Impact of Deep Brain Stimulation of Subthalamic Nucleus on the Hepatic Glucose Production in Parkinson's Disease|
- The primary outcome is the hepatic glucose production determined using the 2H2 glucose enrichment measurement and the infusion flow. [ Time Frame: The hepatic glucose production was calculated during OFF stimulation period and ON stimulation period ]
- -Insulin plasma concentration kinetic -Glucose plasma concentration kinetic -Glucagon plasma concentration kinetic [ Time Frame: During plasma concentration kinetic ]
|Study Start Date:||April 2008|
|Study Completion Date:||June 2008|
|Primary Completion Date:||June 2008 (Final data collection date for primary outcome measure)|
Behavioral: e.g., Protein and calorie controlled diet; Self-hypnotic relaxation
ilot study 8 patients
Inclusion visit :
- Clinical examination/ Interview on health and medical history
- Complete UPDRS
- Body composition measured by DEXA
- Biologic check up
All subjects were studied in the postabsorptive state after a 10-h overnight fast.
On the day of the experiment, patients do not receive their treatment (MED OFF). One catheter was retrogradely inserted into a dorsal vain and was used for blood sample. A second catheter was inserted into the controlateral arm for the tracer infusion. A continuous infusion of D-6,6 2H2 glucose (0,05mg/kg/h) was performed during 6 hours (after a primed dose of 0,05 mg/kg of this tracer).
The first 3 hours, patients were studied without stimulation (STIM OFF); the last 3 hours the stimulator was actuated (STIM ON). Blood samples were regularly collected for the 2H2 glucose enrichment determination, and for the insulin, glucose and glucagon plasma concentration analyses.
Please refer to this study by its ClinicalTrials.gov identifier: NCT00663312
|Clermont-Ferrand, France, 63000|
|Principal Investigator:||Franck Durif, Pr||University Hospital, Clermont-Ferrand|