title: Brain energy consumption induced by electrical stimulation promotes systemic glucose uptake.
abstract: BACKGROUND
  Controlled transcranial stimulation of the brain is part of clinical treatment strategies in neuropsychiatric diseases such as depression, stroke, or Parkinson's disease. Manipulating brain activity by transcranial stimulation, however, inevitably influences other control centers of various neuronal and neurohormonal feedback loops and therefore may concomitantly affect systemic metabolic regulation. Because hypothalamic adenosine triphosphate-sensitive potassium channels, which function as local energy sensors, are centrally involved in the regulation of glucose homeostasis, we tested whether transcranial direct current stimulation (tDCS) causes an excitation-induced transient neuronal energy depletion and thus influences systemic glucose homeostasis and related neuroendocrine mediators.
  
  
  METHODS
  In a crossover design testing 15 healthy male volunteers, we increased neuronal excitation by anodal tDCS versus sham and examined cerebral energy consumption with ³¹phosphorus magnetic resonance spectroscopy. Systemic glucose uptake was determined by euglycemic-hyperinsulinemic glucose clamp, and neurohormonal measurements comprised the parameters of the stress systems.
  
  
  RESULTS
  We found that anodic tDCS-induced neuronal excitation causes an energetic depletion, as quantified by ³¹phosphorus magnetic resonance spectroscopy. Moreover, tDCS-induced cerebral energy consumption promotes systemic glucose tolerance in a standardized euglycemic-hyperinsulinemic glucose clamp procedure and reduces neurohormonal stress axes activity.
  
  
  CONCLUSIONS
  Our data demonstrate that transcranial brain stimulation not only evokes alterations in local neuronal processes but also clearly influences downstream metabolic systems regulated by the brain. The beneficial effects of tDCS on metabolic features may thus qualify brain stimulation as a promising nonpharmacologic therapy option for drug-induced or comorbid metabolic disturbances in various neuropsychiatric diseases.
authors.affiliation: Department of Neurology, University of Lübeck, Lübeck, Germany.
authors.forename: Ferdinand
authors.initials: F
authors.lastname: Binkofski
authors.forename: Michaela
authors.initials: M
authors.lastname: Loebig
authors.forename: Kamila
authors.initials: K
authors.lastname: Jauch-Chara
authors.forename: Sigrid
authors.initials: S
authors.lastname: Bergmann
authors.forename: Uwe H
authors.initials: UH
authors.lastname: Melchert
authors.forename: Harald G
authors.initials: HG
authors.lastname: Scholand-Engler
authors.forename: Ulrich
authors.initials: U
authors.lastname: Schweiger
authors.forename: Luc
authors.initials: L
authors.lastname: Pellerin
authors.forename: Kerstin M
authors.initials: KM
authors.lastname: Oltmanns
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism*; D000324:Adrenocorticotropic Hormone / Q000097:blood; D000328:Adult; D001786:Blood Glucose / Q000378:metabolism; D001794:Blood Pressure / Q000502:physiology; D001921:Brain / Q000378:metabolism*; D004558:Electric Stimulation / Q000379:methods; D004734:Energy Metabolism; D005947:Glucose / Q000378:metabolism*; D005951:Glucose Tolerance Test / Q000379:methods / Q000706:statistics & numerical data; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007328:Insulin / Q000097:blood; D009682:Magnetic Resonance Spectroscopy / Q000379:methods; D008297:Male; D010725:Phosphocreatine / Q000378:metabolism*; D010758:Phosphorus
chemical_list: D001786:Blood Glucose; D007328:Insulin; D010725:Phosphocreatine; D010758:Phosphorus; D000255:Adenosine Triphosphate; D000324:Adrenocorticotropic Hormone; D005947:Glucose; D006854:Hydrocortisone