BLOOD-TO-BRAIN GLUCOSE-TRANSPORT AND CEREBRAL GLUCOSE-METABOLISM ARE NOT REDUCED IN POORLY CONTROLLED TYPE-1 DIABETES

To test the hypothesis that blood-to-brain glucose transport is reduce d in poorly controlled type 1 diabetes, we studied seven patients with a mean (+/- SD) HbA(1c) level of 10.1 +/- 1.2% and nine nondiabetic s ubjects during hyperinsulinemic, mildly hypoglycemic (similar to 3.6 m mol/l, similar to 65 mg/dl) glucose clamps. Blood-to-brain glucose tra nsport and cerebral glucose metabolism mere calculated from rate const ants derived from blood and brain time-activity curves-the latter dete rmined by positron emission tomography (PET)-afterintravenous injectio n of [1-C-11]glucose using a model that includes a fourth rate constan t to account for regional egress of C-11 metabolites. Cerebral blood f low and cerebral blood volume were determined with intravenous (H2O)-O -15 and inhaled (CO)-O-15, respectively, also by PET. At plateau plasm a glucose concentrations of 3.6 +/- 0.0 and 3.7 +/- 0.1 mmol/l, rates of blood-to-brain glucose transport mere similar in the two groups (23 .7 +/- 2.2 and 21.6 +/- 2.9 mu mol.100 g(-1).min(-1), P = 0.569, in th e control subjects and the patients, respectively). There were also no differences in the rates of cerebral glucose metabolism (16.8 +/- 0.8 and 16.3 +/- 1.2 mu mol.100 g(-1).min(-1), P = 0.693, respectively). Plasma epinephrine (1,380 +/- 340 vs. 450 +/- 170 pmol/l, P = 0.0440) and glucagon (26 +/- 5 vs. 12 +/- 1 pmol/l, P = 0.0300) responses to m ild hypoglycemia were reduced in the patients with type 1 diabetes, me conclude that neither blood-to-brain glucose transport nor cerebral g lucose metabolism is measurably reduced in people with poorly controll ed type 1 diabetes.