
2型糖尿病患者前额叶皮质脑损伤与血糖控制
Author(s) -
Choi Sarah E.,
Roy Bhaswati,
Freeby Matthew,
Mullur Rashmi,
Woo Mary A.,
Kumar Rajesh
Publication year - 2020
Publication title -
journal of diabetes
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.949
H-Index - 43
eISSN - 1753-0407
pISSN - 1753-0393
DOI - 10.1111/1753-0407.13019
Subject(s) - glycemic , medicine , prefrontal cortex , voxel , body mass index , diabetes mellitus , magnetic resonance imaging , cognition , nuclear medicine , cardiology , endocrinology , radiology , psychiatry
Background This study examined brain tissue integrity in sites that controls cognition (prefrontal cortices; PFC) and its relationships to glycemic outcomes in adults with type 2 diabetes mellitus (T2DM). Methods We examined 28 T2DM patients (median age 57.1 years; median body mass index [BMI] 30.6 kg/m 2 ;11 males) and 47 healthy controls (median age 55.0 years; median BMI 25.8 kg/m 2 ; 29 males) for cognition (Montreal Cognitive Assessment [MoCA]), glycemic control (hemoglobin A1c [HbA1c]), and PFC tissue status via brain magnetic resonance imaging (MRI). High‐resolution T1‐weighted images were collected using a 3.0‐Tesla MRI scanner, and PFC tissue changes (tissue density) were examined with voxel‐based morphometry procedures. Results Reduced PFC density values were observed in T2DM patients compared to controls (left, 0.41 ± 0.02 mm 3 /voxel vs 0.44 ± 0.02 mm 3 /voxel, P < 0.001; right, 0.41 ± 0.03 mm 3 /voxel vs 0.45 ± 0.02 mm 3 /voxel, P < 0.001). PFC density values were positively correlated with cognition; left PFC region (r = 0.53, P = 0.005) and right PFC region (r = 0.56, P = 0.003), with age and sex as covariates. Significant negative correlations were found between PFC densities and HbA1c values; left PFC region (r = −0.39, P = 0.049) and right PFC region (r = −0.48, P = 0.01), with age and sex as covariates. Conclusions T2DM patients showed PFC brain tissue damage, which is associated with cognitive deficits and poor glycemic control. Further research is needed to identify causal relationships between HbA1c, cognition, and brain changes in T2DM and to evaluate the impact of interventions to prevent brain tissue injury or neuroregeneration in this high‐risk patient population, to eventually preserve or enhance cognition and improve glucose outcomes.