Abnormal Alterations of Cortical Thickness in 16 Patients with Type 2 Diabetes Mellitus: A Pilot MRI Study / 中国医学科学杂志(英文版)

Objective The aim of this study is to investigate the cerebral cortical thickness changes in type 2 diabetes mellitus (T2DM) using a whole brain cortical thickness mapping system based on brain magnetic resonance imaging (MRI).Methods High resolution three-dimensional T1-weighted fast spoiled gradient recalled echo MR images were obtained from 16 patients with T2DM, as well as from 16 normal controls. The whole brain cortical thickness maps were generated, and the cortical thickness of each brain region was calculated according to gyral based regions of interest (ROI) using an automated labeling system by the Freesurfer software. We compared mean cortical thickness at each brain region by the analysis of covariance with age and sex as covariates. The regional difference of the cortical thickness over the whole brain was compared by the analysis of surface-based cortical thickness.Results Mean cortical thicknesses analysis showed bilateral cerebrum in the patients with T2DM (left: 2.52±0.07 mm; right: 2.51±0.08 mm) were significant thinner than those in the normal controls (left: 2.56±0.09 mm; right: 2.56±0.09 mm) (both P<0.05). Regional cortical thinning in T2DM was demonstrated in the paracentral lobule, postcentral gyrus, lateral occipital gyrus, lingual gyrus, precuneus, superior temporal gyrus, middle temporal gyrus, inferior temporal gyrus and posterior cingulate gyrus, compared to the normal controls. The cortical thickness of left middle cingulate and right inferior temporal gyrus were negatively correlated with the disease course.Conclusion A widespread cortical thinning was revealed in patients with T2DM by the analysis of brain cortical thickness on MR. Our finding supports the idea that T2DM could lead to subtle diabetic brain structural changes.

The effects and mechanisms of BTBD10 on the proliferation of islet beta cell / 中华内科杂志

ObjectiveTo explore the role of BTBD10 overexpression in the proliferation of insulinoma cell line INS-1and its mechanism. MethodsThe recombined expression plasmid of pcDNA4.0-BTBD10 was constructed by gene cloning technique and was transfected into INS-1 cell by lipofectamine 2000. The stable overexpression BTBD10 of INS-1cell was selected at 48th hour after transfection.INS-1 cell proliferation activity was measured by MTT method.The expression of BTBD10,protein kinase B(Akt),phospho-Akt(p-Akt),mammal target of rapamycin (mTOR) and phospho-mTOR (p-mTOR) were determined by Western blot.ResultsThe stable overexpression BTBD10 of INS-1 cell wassuccessfullyconstructed.OverproductionofBTBD10promotedbetacellproliferation.The phosphorylation of Akt and mTOR was increased and the ratio of p-Akt/Akt and p-mTOR/mTOR was enhanced in the INS-1 overexpressed by BTBD10.But the expression of total Akt and mTOR presented no obvious changes. Conclusion The overexpression BTBD10 of INS-1 cell could activate of Akt/mTOR signalling pathway via stimulating phospho-mTOR and Akt,and enhance overall cell protein translation,so as to promote proliferation of INS-1 cell.