Animal studies have shown that central
dopamine signaling influences
glucose metabolism. As a first step to show this association in an experimental setting in humans, we studied whether
deep brain stimulation (DBS) of the subthalamic nucleus (STN), which modulates the basal ganglia circuitry, alters basal endogenous
glucose production (EGP) or
insulin sensitivity in patients with
Parkinson's disease (PD). We studied 8 patients with PD treated with DBS STN, in the basal state and during a hyperinsulinemic euglycemic clamp using a stable
glucose isotope, in the stimulated and non-stimulated condition. We measured EGP, hepatic
insulin sensitivity, peripheral
insulin sensitivity (Rd), resting energy expenditure (REE), glucoregulatory
hormones, and Parkinson symptoms, using the Unified Parkinson's Disease Rating Scale (UPDRS). Basal plasma
glucose and EGP did not differ between the stimulated and non-stimulated condition. Hepatic
insulin sensitivity was similar in both conditions and there were no significant differences in Rd and plasma glucoregulatory
hormones between DBS on and DBS off. UPDRS was significantly higher in the non-stimulated condition. DBS of the STN in patients with PD does not influence basal EGP or
insulin sensitivity. These results suggest that acute modulation of the motor basal ganglia circuitry does not affect
glucose metabolism in humans.