期刊
DIABETES CARE
卷 35, 期 12, 页码 2570-2574出版社
AMER DIABETES ASSOC
DOI: 10.2337/dc12-0297
关键词
-
资金
- National Institutes of Health (NIH) [R37 DK27085, MO1 RR00036, UL1 RR24992, P60 DK20579]
- Washington University in St. Louis
- NIH [UL1RR024992]
OBJECTIVE-The central nervous system mechanisms of defenses against falling plasma glucose concentrations, and how they go awry and result in iatrogenic hypoglycemia in diabetes, are not known. Hypoglycemic plasma glucose concentrations of 55 mg/dL (3.0 mmol/L) cause symptoms, activate glucose counterregulatory systems, and increase synaptic activity in a network of brain regions including the dorsal midline thalamus in humans. We tested the hypothesis that slightly subphysiological plasma glucose concentrations of 65 mg/dL (3.6 mmol/L), which do not cause symptoms but do activate glucose counterregulatory systems, also activate brain synaptic activities. RESEARCH DESIGN ANDMETHODS-We measured relative regional cerebral blood flow (rCBF), an index of synaptic activity, in predefined brain regions with [O-15] water positron emission tomography, symptoms, and plasma epinephrine and glucagon concentrations during a 2-h euglycemic (90 mg/dL) to hypoglycemic (55 mg/dL) clamp (n = 20) or a 2-h euglycemic to slight subphysiological (65 mg/dL) clamp (n = 9) in healthy humans. RESULTS-Clamped plasma glucose concentrations of 65 mg/dL did not cause hypoglycemic symptoms, but raised plasma epinephrine and glucagon concentrations and increased rCBF (P = 0.007) only in the dorsal midline thalamus. CONCLUSIONS-Slightly subphysiological plasma glucose concentrations increase synaptic activity in the dorsal midline thalamus in humans.
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