Abstract
Background: Glucose alterations are associated with impaired cognition. The 1-h-post-load plasma glucose ≥155 mg/dl in non-diabetic subjects confers an increased risk of cardiovascular events and diabetes. This pilot study aimed to investigate whether the 1-h-post-load plasma glucose ≥155 mg/dl negatively affects the subcortical regions of the brain and the cognitive functions.Methods: We enrolled 32 non-diabetic subjects. Patients were divided into two groups based on 1-h- post-load plasma glucose value > or < 155 mg/dl: normal glucose tolerance (NGT) 1-h-high and NGT 1-h-low subjects. All subjects underwent 3 Tesla MRI and standard neuropsychological tests.Results: NGT 1-h-high subjects showed significantly lower values of both right (4.9 ± 0.9 vs. 5.1 ± 0.9 ml) and left (4.8 ± 1.1 vs. 5.1 ± 1.1 ml) hippocampal hemisphere volume, while right hemisphere hippocampal diffusivity was lower in the NGT 1-h-high group (10.0 ± 0.6 vs. 10.6 ± 0.5 10−4 mm2s−1). NGT 1-h-high subjects also showed a poorer memory performance. In particular, for both Rey Auditory Verbal Learning Task (RAVLT)—immediate-recall and Free and Cued Selective Reminding Test (FCSRT)—delayed total recall, we found lower cognitive test scores in the NGT-1 h-high group (26.5 ± 6.3 and 10.4 ± 0.3, respectively).Conclusions: One-hour-post-load hyperglycemia is associated with morpho-functional subcortical brain alterations and poor memory performance tests.
Highlights
Alterations of glucose metabolism, in particular impaired glucose tolerance (IGT) and type 2 diabetes mellitus (T2DM), have been associated with an increased incidence of Alzheimer’s disease (AD) and vascular dementia (Exalto et al, 2012)
Evidence indicates that the cognitive impairment commonly seen in many prediabetic/diabetic patients can be mediated by an altered signaling insulin-like growth factor (IGF) 1-insulin (Ye et al, 2002; Talbot et al, 2012)
We demonstrated that glucose normotolerant subjects who exhibit plasma glucose levels ≥155 mg/dl 1-h after an oral load of 75 g of glucose [normal glucose tolerance (NGT 1-h-high)] have a high prevalence of subclinical target organ damage; in particular, these subjects are characterized by an unfavorable CV risk profile (Succurro et al, 2009, 2010; Fiorentino et al, 2016) and are at an increased risk for future T2DM development (Fiorentino et al, 2015)
Summary
Alterations of glucose metabolism, in particular impaired glucose tolerance (IGT) and type 2 diabetes mellitus (T2DM), have been associated with an increased incidence of Alzheimer’s disease (AD) and vascular dementia (Exalto et al, 2012). Evidence indicates that the cognitive impairment commonly seen in many prediabetic/diabetic patients can be mediated by an altered signaling insulin-like growth factor (IGF) 1-insulin (Ye et al, 2002; Talbot et al, 2012). The 1-h-post-load plasma glucose ≥155 mg/dl in non-diabetic subjects confers an increased risk of cardiovascular events and diabetes This pilot study aimed to investigate whether the 1-h-post-load plasma glucose ≥155 mg/dl negatively affects the subcortical regions of the brain and the cognitive functions
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