Impact of Deep Brain Stimulation of Subthalamic Nucleus on the Hepatic Glucose Production in Parkinson's Disease

Not Applicable

Terminated

• Conditions: Idiopathic Parkinson's Disease

• Registration Number: NCT00663312
• Lead Sponsor: University Hospital, Clermont-Ferrand

Brief Summary

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.

Detailed Description

ilot study 8 patients

Inclusion visit :

* Clinical examination/ Interview on health and medical history

* Complete UPDRS

* Body composition measured by DEXA

* Biologic check up

* MMS

Protocol :

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.

Study Timeline

• Study Start: 2008-04
• Study First Submitted: 2008-04-14
• Study First Submitted QC: 2008-04-21
• Study First Posted: 2008-04-22
• Primary Completion: 2008-06
• Study Completion: 2008-06
• Status Verified: 2008-10
• Last Update Submitted: 2008-10-07
• Last Update Posted: 2008-10-08

Recruitment & Eligibility

• Status: TERMINATED
• Sex: All
• Target Recruitment: 8

Inclusion Criteria

Not provided

Exclusion Criteria

Not provided

Study & Design

• Study Type: INTERVENTIONAL
• Study Design: CROSSOVER

Primary Outcome Measures

Name	Time	Method
The primary outcome is the hepatic glucose production determined using the 2H2 glucose enrichment measurement and the infusion flow.	The hepatic glucose production was calculated during OFF stimulation period and ON stimulation period

Secondary Outcome Measures

Name	Time	Method
-Insulin plasma concentration kinetic -Glucose plasma concentration kinetic -Glucagon plasma concentration kinetic	During plasma concentration kinetic

Trial Locations

Locations (1)

CHU; 🇫🇷 Clermont-Ferrand, France