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. 2018 Apr 19:10.1111/pedi.12683.
doi: 10.1111/pedi.12683. Online ahead of print.

Longitudinal assessment of hippocampus structure in children with type 1 diabetes

Lara C Foland-Ross  1 , Allan L Reiss  1   2   3 , Paul K Mazaika  1 , Nelly Mauras  4 , Stuart A Weinzimer  5 , Tandy Aye  1   6 , Michael J Tansey  7 , Neil H White  8 ; Diabetes Research in Children Network (DirecNet)
Affiliations

Longitudinal assessment of hippocampus structure in children with type 1 diabetes

Lara C Foland-Ross et al. Pediatr Diabetes. .

Abstract

The extant literature finds that children with type 1 diabetes mellitus (T1D) experience mild cognitive alterations compared to healthy age-matched controls. The neural basis of these cognitive differences is unclear but may relate in part to the effects of dysglycemia on the developing brain. We investigated longitudinal changes in hippocampus volume in young children with early-onset T1D. Structural magnetic resonance imaging data were acquired from 142 children with T1D and 65 age-matched control subjects (4-10 years of age at study entry) at 2 time points, 18 months apart. The effects of diabetes and glycemic exposure on hippocampal volume and growth were examined. Results indicated that although longitudinal hippocampus growth did not differ between children with T1D and healthy control children, slower growth of the hippocampus was associated with both increased exposure to hyperglycemia (interval HbA1c) and greater glycemic variability (MAGE) in T1D. These observations indicate that the current practice of tolerating some hyperglycemia to minimize the risk of hypoglycemia in young children with T1D may not be optimal for the developing brain. Efforts that continue to assess the factors influencing neural and cognitive development in children with T1D will be critical in minimizing the deleterious effects of diabetes.

Keywords: blood glucose; brain; hippocampus; hyperglycemia; type 1 diabetes mellitus.

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Conflict of interest statement

Conflict of Interest

S.A.W. reports receiving consulting fees from Insulet and payment to his institution from a Medtronic grant. N.H.W. has received payment for consultancy from Novo Nordisk and Daiichi Sankyo. N.M. reports a research device supply agreement with her institution from Medtronic and Lifescan and research grant support from Medtronic, and consultancy from PicoLife Technologies. TA reports payment to her institution from a Medtronic Grant. No other potential conflicts of interest relevant to this article were reported.

Figures

Figure 1
Figure 1
Mean volume of the hippocampus (averaged across hemispheres and time points), adjusted for age at baseline and total brain volume. Error bars represent standard deviation. *p < 0.05.
Figure 2
Figure 2
Associations between change in hippocampus volume from time 1 to time 2 and total exposure to hyperglycemia (incremental change in HbA1cAUC6%, left), mean amplitude of glycemic excursions (MAGE, middle) and mean blood glucose (avgMean, right) experienced between these two time points. Values are adjusted for covariates in the model (see text).
See this image and copyright information in PMC

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