10.5061/DRYAD.WSTQJQ2H0
Bednařík, Petr
0000-0002-8828-7661
Medical University of Vienna
Henry, Pierre Gilles
University of Minnesota
Khowaja, Ameer
University of Minnesota
Rubin, Nathan
University of Minnesota
Kumar, Anjali
University of Minnesota
Deelchand, Dinesh
University of Minnesota
Eberly, Lynn
University of Minnesota
Seaquist, Elizabeth
University of Minnesota
Öz, Gülin
University of Minnesota
Amir, Moheet
University of Minnesota
Supplement to: Hippocampal neurochemical profile and glucose transport
kinetics in patients with type 1 diabetes
Dryad
dataset
2020
Clinical and Translational Science Institute
KL2TR000113
National Institute of Neurological Disorders and Stroke
https://ror.org/01s5ya894
R01 NS035192,P41 EB015894,P30 NS076408,S10 OD017974
Brain & Behavior Research Foundation
https://ror.org/03a63f080
27,238,846,793
Marie Skłodowska-Curie
846793
2020-02-04T00:00:00Z
2020-02-04T00:00:00Z
en
https://doi.org/10.1210/clinem/dgz062
2515626 bytes
2
CC0 1.0 Universal (CC0 1.0) Public Domain Dedication
Context Longstanding type 1 diabetes (T1D) may lead to alterations in
hippocampal neurochemical profile. Upregulation of hippocampal glucose
transport as a result of recurrent exposure to hypoglycemia may preserve
cognitive function during future hypoglycemia in subjects with T1D and
impaired awareness of hypoglycemia (IAH). The effect of T1D on hippocampal
neurochemical profile and glucose transport is unknown. Objective To test
the hypothesis that hippocampal neurochemical composition is altered in
T1D and glucose transport is upregulated in T1D with IAH. Design and
participants Hippocampal neurochemical profile was measured with
single-voxel magnetic resonance spectroscopy at 3T during euglycemia in 18
healthy controls (HC), 10 T1D with IAH, and 12 T1D with normal awareness
to hypoglycemia (NAH). Additionally, 12 HC, 8 T1D-IAH, and 6 T1D-NAH were
scanned during hyperglycemia to assess hippocampal glucose transport with
metabolic modeling. Setting University medical center. Main Outcome
Measures Concentrations of hippocampal neurochemicals measured during
euglycemia and ratios of maximal transport rate to cerebral metabolic rate
of glucose (Tmax/CMRGlc), derived from magnetic resonance
spectroscopy–measured hippocampal glucose as a function of plasma glucose.
Results Comparison of hippocampal neurochemical profile revealed no group
differences (HC, T1D, T1D-IAH, and T1D-NAH). The ratio Tmax/CMRGlc was not
significantly different between the groups, T1D-IAH (1.58 ± 0.09) and HC
(1.65 ± 0.07, P = 0.54), between T1D-NAH (1.50 ± 0.09) and HC (P = 0.19),
and between T1D-IAH and T1D-NAH (P = 0.53). Conclusions Subjects with T1D
with sufficient exposure to recurrent hypoglycemia to create IAH did not
have alteration of Tmax/CMRglc or neurochemical profile compared with
participants with T1D-NAH or HC.
Suppemental figures and tables.