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Supplement to: Hippocampal neurochemical profile and glucose transport kinetics in patients with type 1 diabetes

Citation

Bednařík, Petr et al. (2020), Supplement to: Hippocampal neurochemical profile and glucose transport kinetics in patients with type 1 diabetes, Dryad, Dataset, https://doi.org/10.5061/dryad.wstqjq2h0

Abstract

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.

Usage Notes

Suppemental figures and tables.

Funding

Clinical and Translational Science Institute, Award: KL2TR000113

National Institutes of Health, Award: R01 NS035192,P41 EB015894,P30 NS076408,S10 OD017974

Brain and Behavior Research Foundation, Award: 27,238,846,793

Marie Skłodowska-Curie, Award: 846793