Literature DB >> 23633215

Deep brain stimulation of the subthalamic nucleus regulates postabsorptive glucose metabolism in patients with Parkinson's disease.

Marie Batisse-Lignier1, Isabelle Rieu, Christelle Guillet, Estelle Pujos, Béatrice Morio, Jean-Jacques Lemaire, Franck Durif, Yves Boirie.   

Abstract

OBJECTIVE: Subthalamic nucleus-deep brain stimulation (STN-DBS) is an alternative treatment for patients with uncontrolled symptoms of Parkinson's disease (PD), but it has other nonmotor impact. Because STN-DBS alters the energy expenditure in humans, we hypothesized that STN-DBS may affect postabsorptive glucose metabolism in patients with PD. RESEARCH DESIGN AND METHODS: Endogenous glucose production (EGP) and whole-body glucose disposal rates (GDRs) were assessed in the postabsorptive state during a primed continuous iv infusion of D-[6,6-(2)H2]glucose for 5 hours in 8 STN-DBS-treated patients with PD, without (Stim-OFF) and during STN-DBS (Stim-ON) treatment. EGP and GDR in PD patients were compared with glucose kinetics of 8 matched healthy control subjects. Plasma concentrations of insulin, glucagon, and free fatty acids were also determined.
RESULTS: EGP and GDR were higher in PD patients in Stim-OFF conditions than in the control group (2.62 ± 0.09 vs 2.27 ± 0.10 mg/kg·min, P < .05). Despite no significant changes in blood glucose throughout the kinetic study, a significant and consistent 22% decrease in EGP occurred in PD patients during Stim-ON (2.04 ± 0.07 mg/kg(-1)·min(-1); P < .01), and whole-body glucose kinetics in Stim-ON patients were no more different from those of the control subjects (P = NS). No difference in insulin, glucagon, or free fatty acid concentrations was observed in the patients between Stim-OFF and Stim-ON conditions.
CONCLUSIONS: Deep brain stimulation in patients with PD affects EGP glucose disposal, suggesting that a cross talk between the central nervous system and peripheral tissues may regulate glucose homeostasis.

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Year:  2013        PMID: 23633215     DOI: 10.1210/jc.2012-3838

Source DB:  PubMed          Journal:  J Clin Endocrinol Metab        ISSN: 0021-972X            Impact factor:   5.958


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