Deep Brain Stimulation of the Subthalamic Nucleus Regulates Postabsorptive Glucose Metabolism in Patients With Parkinson's Disease

Batisse-Lignier, Marie; Rieu, Isabelle; Guillet, Christelle; Pujos, Estelle; Morio, Béatrice; Lemaire, Jean‐Jacques; Durif, Franck; Boirie‌, Yves

doi:10.1210/jc.2012-3838

Cited by 19 publications

(15 citation statements)

References 22 publications

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“…Our results seem in contrast with an earlier report on lower EGP upon STN DBS, i.e., Batisse-Lignier et al showed that basal EGP was decreased in the stimulated condition (Batisse-Lignier et al, 2013). However, the 22% decrease in EGP in that study could alternatively be explained by the physiological adaptation to fasting since EGP was measured in both the non-stimulated and stimulated condition, consecutively on one study day, and thus with a difference in hours of fasting.…”

Section: Discussioncontrasting

confidence: 99%

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Subthalamic nucleus stimulation does not influence basal glucose metabolism or insulin sensitivity in patients with Parkinson's disease

et al. 2014

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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.

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Section: Discussioncontrasting

confidence: 99%

“…Studies on glucose metabolism in patients with PD and DBS are scarce. One study showed a reduction in endogenous glucose production (EGP) with STN DBS (Batisse-Lignier et al, 2013). …”

Section: Introductionmentioning

confidence: 99%

Subthalamic nucleus stimulation does not influence basal glucose metabolism or insulin sensitivity in patients with Parkinson's disease

et al. 2014

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“…Some subsequent studies showed an acute rise in blood glucose levels 20 minutes after electroconvulsive therapy application in diabetic and non‐diabetic patients . Furthermore, Batisse‐Lignier et al observed a decrease in endogenous glucose production upon deep brain stimulation in Parkinson's disease, confirming the assumption of communication between the central nervous system and peripheral tissues, which may regulate systemic glucose homeostasis. The results of these studies suggest that direct current‐induced modulation of brain functioning not only affects the brain itself, but also exerts a significant further influence on a number of peripheral functions.…”

Section: Discussionmentioning

confidence: 92%

Double transcranial direct current stimulation of the brain increases cerebral energy levels and systemic glucose tolerance in men

Wardzinski¹,

Friedrichsen²,

Dannenberger³

et al. 2019

J Neuroendocrinology

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Transcranial direct current stimulation (tDCS) is a neuromodulatory method that has been tested experimentally and has already been used as an adjuvant therapeutic option to treat a number of neurological disorders and neuropsychiatric diseases. Beyond its well known local effects within the brain, tDCS also transiently promotes systemic glucose uptake and reduces the activity of the neurohormonal stress axes. We aimed to test whether the effects of a single tDCS application could be replicated upon double stimulation to persistently improve systemic glucose tolerance and stress axes activity in humans. In a single‐blinded cross‐over study, we examined 15 healthy male volunteers. Anodal tDCS vs sham was applied twice in series. Systemic glucose tolerance was investigated by the standard hyperinsulinaemic‐euglycaemic glucose clamp procedure, and parameters of neurohormonal stress axes activity were measured. Because tDCS‐induced brain energy consumption has been shown to be part of the mechanism underlying the assumed effects, we monitored the cerebral high‐energy phosphates ATP and phosphocreatine by 31phosphorus magnetic resonance spectroscopy. As hypothesised, analyses revealed that double anodal tDCS persistently increases glucose tolerance compared to sham. Moreover, we observed a significant rise in cerebral high‐energy phosphate content upon double tDCS. Accordingly, the activity of the neurohormonal stress axes was reduced upon tDCS compared to sham. Our data demonstrate that double tDCS promotes systemic glucose uptake and reduces stress axes activity in healthy humans. These effects suggest that repetitive tDCS may be a future non‐pharmacological option for combating glucose intolerance in type 2 diabetes patients.

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“…Furthermore, motor improvement actually may help protect against WG in STN‐stimulated patients, because the increase in physical activity made possible by newly acquired motor abilities counterbalances the reduction in energy expenditure arising from the alleviation of motor symptoms . Alternatively, DBS has been hypothesized to affect the central regulation of eating behavior or energy metabolism . Decreased energy expenditure has thus been attributed either to motor improvements or to action on the centers that control metabolism …”

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confidence: 99%

Weight gain following subthalamic nucleus deep brain stimulation: A PET study

et al. 2014

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Several hypotheses have been put forward to explain weight gain after deep brain stimulation (DBS), but none provides a fully satisfactory account of this adverse effect. We analyzed the correlation between changes in brain metabolism (using positron emission tomography [PET] imaging) and weight gain after bilateral subthalamic nucleus DBS in patients with Parkinson's disease. Body mass index was calculated and brain activity prospectively measured using 2-deoxy-2[18F]fluoro-D-glucose 3 months before and 4 months after the start of subthalamic nucleus deep brain stimulation in 23 patients with Parkinson's disease. Motor complications (United Parkinson's Disease Rating Scale [UPDRS]-IV scores) and dopaminergic medication were included in the analysis to control for their possible influence on brain metabolism. Mean ± standard deviation (SD) body mass index increased significantly by 0.8 ± 1.5 kg/m(2) (P = 0.03). Correlations were found between weight gain and changes in brain metabolism in limbic and associative areas, including the orbitofrontal cortex (Brodmann areas [BAs] 10 and 11), lateral and medial parts of the temporal lobe (BAs 20, 21, 22,39 and 42), anterior cingulate cortex (BA 32), and retrosplenial cortex (BA 30). However, we found no correlation between weight gain and metabolic changes in sensorimotor areas. These findings suggest that changes in associative and limbic processes contribute to weight gain after subthalamic nucleus DBS in Parkinson's disease.

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Deep Brain Stimulation of the Subthalamic Nucleus Regulates Postabsorptive Glucose Metabolism in Patients With Parkinson's Disease

Abstract: 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.

Cited by 19 publications

References 22 publications

Subthalamic nucleus stimulation does not influence basal glucose metabolism or insulin sensitivity in patients with Parkinson's disease

Subthalamic nucleus stimulation does not influence basal glucose metabolism or insulin sensitivity in patients with Parkinson's disease

Double transcranial direct current stimulation of the brain increases cerebral energy levels and systemic glucose tolerance in men

Weight gain following subthalamic nucleus deep brain stimulation: A PET study

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