Journal
DIABETES
Volume 57, Issue 2, Pages 470-475Publisher
AMER DIABETES ASSOC
DOI: 10.2337/db07-1329
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Funding
- NCRR NIH HHS [MO1 RR00036, M01 RR000036-475228, M01 RR000036] Funding Source: Medline
- NIDDK NIH HHS [R37 DK27085, P60 DK020579, K12 DK063683, P60 DK20579, P60 DK020579-31, R37 DK027085-27, K12 DK63683, R37 DK027085] Funding Source: Medline
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OBJECTIVE-Hypoglycemia, the limiting factor in the glycemic management of diabetes, is the result of the interplay of therapeutic insulin excess and compromised glycemic defenses. The key feature of the latter is an attenuated sympathoadrenal response to hypoglycemia that typically follows an episode of recent antecedent iatrogenic hypoglycemia, a phenomenon termed hypoglycemia-associated autonomic failure (HAAF) in diabetes. We investigated the role of cerebral mechanisms in HAAF by measuring regional brain activation during recurrent hypoglycemia with attenuated counterregulatory responses and compaxing it with initial hypoglycemia in healthy individuals. RESEARCH DESIGN AND METHODS-We used [O-15]water and positron emission tomography to measure regional cerebral blood flow as a marker of brain synaptic activity during hyper-insulinemic hypoglycemic clamps (55 mg/dl (3.0 mmol/l]) in the naive condition (day 1) and after similar to 24 h of interval interprandial hypoglycemia (day 2) in nine healthy adults. RESULTS-Interval hypoglycemia produced attenuated sympathoadrenal, symptomatic, and other counterregulatory responses to hypoglycemia on day 2, a model of HAAF. Synaptic activity in the dorsal midline thalamus during hypoglycemia was significantly greater on day 2 than day 1 (P = 0.004). CONCLUSIONS-Greater synaptic activity associated with attenuated counterregulatory responses indicates that the dorsal midline thalamus plays an active inhibitory role in reducing sympathoadrenal and symptomatic responses to hypoglycemia when previous hypoglycemia has occurred, the key feature of HAAF in diabetes.
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