Key result
Compared with lean controls, obese T2DM patients showed lower right insula thickness and left lateral occipital surface area, while normoglycemic obese subjects had lower right insula thickness but higher amygdala and thalamus volume.
Why the study?
Do obesity and type 2 diabetes alter cortical and subcortical gray matter structure compared to lean normoglycemic controls?
Cross-Sectional (n=75)
No
Do obesity and type 2 diabetes alter cortical and subcortical gray matter structure compared to lean normoglycemic controls?
p-value: p=<0.05
Parietal and occipital structural deficits may represent early T2DM-related cerebral alterations, whereas normoglycemic obesity affects regions involved in emotion, appetite, and satiety regulation.
Distinct cortical patterns distinguish obese T2DM from normoglycemic obesity; leaves open whether diabetes drives early parietal-occipital changes.
Type 2 diabetes (T2DM) is associated with structural cortical and subcortical alterations, although it is insufficiently clear if these alterations are driven by obesity or by diabetes and its associated complications. We used FreeSurfer5.3 and FSL-FIRST to determine cortical thickness, volume and surface area, and subcortical gray matter volume in a group of 16 normoglycemic obese subjects and 28 obese T2DM patients without clinically manifest micro- and marcoangiopathy, and compared them to 31 lean normoglycemic controls. Forward regression analysis was used to determine demographic and clinical correlates of altered (sub)cortical structure. Exploratively, vertex-wise correlations between cortical structure and fasting glucose and insulin were calculated. Compared with controls, obese T2DM patients showed lower right insula thickness and lower left lateral occipital surface area ( P FWE < 0.05). Normoglycemic obese versus controls had lower thickness ( P FWE < 0.05) in the right insula and inferior frontal gyrus, and higher amygdala and thalamus volume. Thalamus volume and left paracentral surface area were also higher in this group compared with obese T2DM patients. Age, sex, BMI, fasting glucose, and cholesterol were related to these (sub)cortical alterations in the whole group (all P < 0.05). Insulin were related to temporal and frontal structural deficits (all P FWE < 0.05). Parietal/occipital structural deficits may constitute early T2DM-related cerebral alterations, whereas in normoglycemic obese subjects, regions involved in emotion, appetite, satiety regulation, and inhibition were affected. Central adiposity and elevated fasting glucose may constitute risk factors.
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Bernardes et al. (2018) conducted a cross-sectional in Obesity and Type 2 Diabetes (n=75). Obesity and Type 2 Diabetes vs. Lean normoglycemic controls was evaluated on Cortical thickness, surface area, and subcortical gray matter volume (p=<0.05). Compared with lean controls, obese T2DM patients showed lower right insula thickness and left lateral occipital surface area, while normoglycemic obese subjects had lower right insula thickness but higher amygdala and thalamus volume.
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