Background: DNA methylation inhibits gene expression by preventing transcription factors from binding to DNA. Functioning of nigrostriatal dopaminergic neurons is influenced by the expression of the dopamine transporter (DAT), and genetic variations in the gene encoding DAT contribute to differences in reward processing. We aimed to investigate the action of DAT methylation on DAT protein expression measured by positron emission tomography (PET). Methods: The emission data were acquired over 90 min with 50 frames after injection of ¹⁸F-FP-CIT using PET. Binding potentials (BP_NDs) of ventral striatum, caudate nucleus, putamen were measured with the simplified reference tissue method. Genomic DNA was extracted from subjects’ blood sampling. Methylation of 4 regions in SLC6A3 gene was assessed using bisulfite pyrosequencing. The mean percentage of methylation (%) for each cluster was calculated by taking the average of all CpG site methylation levels measured within the cluster. Subjects were assessed with the Generalized Reward and Punishment Expectancy Scales (GRAPES) that consists of 30 items related with the reward and punishment that individuals expect for their behaviors. Results: Thirty-five healthy males, with an age range between 20 and 30 years, and a mean age of 24.4 ± 2.7 years, were included in this study. The mean percentage of methylation (%) from cluster C showed a trend of positive correlation with DAT availability of ventral striatum (rho = 0.3712, p = 0.0281), not significant after correction for multiple comparisons, and a significant correlation with GRAPES A: reward expectancy scale (rho = 0.7178, p < 0.0001). Conclusion: DAT methylation from peripheral blood showed a trend of positive correlation with DAT availability of ventral striatum in healthy subjects; however, it was not significant after correction for multiple comparison. The degrees of methylation from cluster C of DAT in peripheral blood were significantly correlated with reward scales of GRAPES A: reward expectancy scale. The association between DAT methylation and DAT expression needs to be investigated further.

The purpose of this study was to evaluate the differences in cerebral glucose metabolism and metabolic connectivity between noise-induced hearing loss (NIHL) subjects and normal subjects. Eighty-nine subjects who needed close observation for NIHL or were diagnosed with NIHL and 89 normal subjects were enrolled. After pre-processing of positron emission tomography images including co-registration, spatial normalization, and smoothing, a two-sample t-test was conducted to compare cerebral glucose metabolism between the two groups. To evaluate metabolic connectivity between two groups, BRAPH–BRain Analysis using graPH theory, a software package to perform graph theory analysis of the brain connectome was used. NIHL subjects showed hypometabolism compared to normal subjects in both insulae (x − 38, y − 18, z 4; × 42, y − 12, z 4) and right superior temporal gyrus (× 44, y 16, z − 20). No brain regions showed hypermetabolism in the NIHL subjects. In metabolic connectivity analysis, NIHL subjects showed decreased average strength, global efficiency, local efficiency, and mean clustering coefficient when compared with normal subjects. Decreased glucose metabolism and metabolic connectivity in NIHL subject might reflect decreased auditory function. It might be characteristic of sensorineural hearing loss.

We evaluated the effects of obesity and osteocalcin on glucose metabolism in the brain. A total of 179 healthy men were enrolled in this study. After preprocessing positron emission tomography images, including by performing coregistration, spatial normalization, and smoothing, regression analysis was conducted to identify the correlation between body mass index, osteocalcin, and brain glucose metabolism. Body mass index was positively correlated with brain glucose metabolism in the anterior lobe of the right cerebellum, the anterior and posterior lobes of the left cerebellum, the right middle frontal gyrus (Brodmann area 9), the right cingulate gyrus (Brodmann area 32), the right anterior cingulate (Brodmann area 32), the left middle frontal gyrus (Brodmann area 10), and the subgyral area of the left frontal lobe. Osteocalcin was negatively correlated with glucose metabolism in the anterior lobe of the left cerebellum. Body mass index was positively correlated with brain glucose metabolism in the prefrontal cortex and cerebellum. Osteocalcin levels were negatively correlated with brain glucose metabolism in the left cerebellum.