title: Blood-to-brain glucose transport and cerebral glucose metabolism are not reduced in poorly controlled type 1 diabetes.
abstract: To test the hypothesis that blood-to-brain glucose transport is reduced in poorly controlled type 1 diabetes, we studied seven patients with a mean (+/- SD) HbA1c level of 10.1 +/- 1.2% and nine nondiabetic subjects during hyperinsulinemic, mildly hypoglycemic (approximately 3.6 mmol/l, approximately 65 mg/dl) glucose clamps. Blood-to-brain glucose transport and cerebral glucose metabolism were calculated from rate constants derived from blood and brain time-activity curves--the latter determined by positron emission tomography (PET)--after intravenous injection of [1-(11)C]glucose using a model that includes a fourth rate constant to account for regional egress of 11C metabolites. Cerebral blood flow and cerebral blood volume were determined with intravenous H2(15)O and inhaled C(15)O, respectively, also by PET. At plateau plasma glucose concentrations of 3.6 +/- 0.0 and 3.7 +/- 0.1 mmol/l, rates of blood-to-brain glucose transport were similar in the two groups (23.7 +/- 2.2 and 21.6 +/- 2.9 micromol x 100 g(-1) x min(-1), P = 0.569, in the 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 micromol x 100 g(-1) x 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 mild hypoglycemia were reduced in the patients with type 1 diabetes. We conclude that neither blood-to-brain glucose transport nor cerebral glucose metabolism is measurably reduced in people with poorly controlled type 1 diabetes.
authors.affiliation: Department of Medicine, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
authors.forename: C G
authors.initials: CG
authors.lastname: Fanelli
authors.forename: C S
authors.initials: CS
authors.lastname: Dence
authors.forename: J
authors.initials: J
authors.lastname: Markham
authors.forename: T O
authors.initials: TO
authors.lastname: Videen
authors.forename: D S
authors.initials: DS
authors.lastname: Paramore
authors.forename: P E
authors.initials: PE
authors.lastname: Cryer
authors.forename: W J
authors.initials: WJ
authors.lastname: Powers
mesh_terms: D000328:Adult; D001786:Blood Glucose / Q000378:metabolism*; D001794:Blood Pressure; D001812:Blood-Brain Barrier; D002250:Carbon Radioisotopes / Q000493:pharmacokinetics; D003922:Diabetes Mellitus, Type 1 / Q000097:blood / Q000378:metabolism* / Q000503:physiopathology; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005260:Female; D005934:Glucagon / Q000097:blood; D005947:Glucose / Q000378:metabolism*; D015309:Glucose Clamp Technique; D006442:Glycated Hemoglobin / Q000032:analysis; D006339:Heart Rate; D019382:Human Growth Hormone / Q000097:blood; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007328:Insulin / Q000097:blood; D008297:Male; D009638:Norepinephrine / Q000097:blood; D010191:Pancreatic Polypeptide / Q000097:blood; D012016:Reference Values; D014055:Tomography, Emission-Computed
chemical_list: D001786:Blood Glucose; D002250:Carbon Radioisotopes; D005230:Fatty Acids, Nonesterified; D005934:Glucagon; D005947:Glucose; D006442:Glycated Hemoglobin; D019382:Human Growth Hormone; D006854:Hydrocortisone; D007328:Insulin; D009638:Norepinephrine; D010191:Pancreatic Polypeptide