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Cerebellar Glucose During Fasting and Acute Hyperglycemia in Nondiabetic Men and in Men with Type 1 Diabetes
Authors:Outi Heikkilä  Sari Mäkimattila  Marjut Timonen  Per-Henrik Groop  Sami Heikkinen  Nina Lundbom
Institution:1.Folkh?lsan Institute of Genetics, Folkh?lsan Research Center,Biomedicum Helsinki, University of Helsinki,Helsinki,Finland;2.Division of Nephrology, Department of Medicine,Helsinki University Hospital,Helsinki,Finland;3.Helsinki Medical Imaging Center,University of Helsinki,Helsinki,Finland;4.Department of Physics,University of Helsinki,Helsinki,Finland;5.Laboratory of Organic Chemistry,University of Helsinki,Helsinki,Finland
Abstract:In diabetic patients, proton magnetic resonance spectroscopy (1H MRS) has revealed increased brain glucose concentration and metabolite alterations that indicate neuronal damage and glial cell activation. Cerebellum is known to be more resistant to hypoglycemia than cerebrum, but the effects of both chronic and acute hyperglycemia on the cerebellum are less well known. 1H MRS was used to quantify brain glucose and metabolite levels in the cerebellum, cerebral cortex, cerebral white matter, and the thalamus of diabetic and nondiabetic men after an overnight fast and during a hyperglycemic normoinsulinemic clamp with blood glucose 12 mmol/l above baseline. Fasting glucose levels were twice as high in the cerebellum than in the cerebrum. During acute hyperglycemia, the cerebellar glucose concentration increased by 3.0 mmol/l, which equals that in the cortex, but is 35% more than in the thalamus and 173% more than in the white matter. Acute hyperglycemia also increased the cerebellar tissue water content by 10%. There were no differences between diabetic and nondiabetic participants. Notably, the patients with complication free type 1 diabetes showed brain metabolite alterations in the cerebral cortex and the white matter but not in the cerebellum. Our study suggests that diabetes does not alter glucose content or uptake in the cerebellum. The increase in tissue water during acute hyperglycemia may serve to protect the cerebellum from the potentially deleterious effects of the excess glucose.
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