ABSTRACT
Background@#CycloZ, a combination of cyclo-His-Pro and zinc, has anti-diabetic activity. However, its exact mode of action remains to be elucidated. @*Methods@#KK-Ay mice, a type 2 diabetes mellitus (T2DM) model, were administered CycloZ either as a preventive intervention, or as a therapy. Glycemic control was evaluated using the oral glucose tolerance test (OGTT), and glycosylated hemoglobin (HbA1c) levels. Liver and visceral adipose tissues (VATs) were used for histological evaluation, gene expression analysis, and protein expression analysis. @*Results@#CycloZ administration improved glycemic control in KK-Ay mice in both prophylactic and therapeutic studies. Lysine acetylation of peroxisome proliferator-activated receptor gamma coactivator 1-alpha, liver kinase B1, and nuclear factor-κB p65 was decreased in the liver and VATs in CycloZ-treated mice. In addition, CycloZ treatment improved mitochondrial function, lipid oxidation, and inflammation in the liver and VATs of mice. CycloZ treatment also increased the level of β-nicotinamide adenine dinucleotide (NAD+), which affected the activity of deacetylases, such as sirtuin 1 (Sirt1). @*Conclusion@#Our findings suggest that the beneficial effects of CycloZ on diabetes and obesity occur through increased NAD+ synthesis, which modulates Sirt1 deacetylase activity in the liver and VATs. Given that the mode of action of an NAD+ booster or Sirt1 deacetylase activator is different from that of traditional T2DM drugs, CycloZ would be considered a novel therapeutic option for the treatment of T2DM.
ABSTRACT
OBJECTIVES: To compare the white matter microstructure of dyslexic children with normal children using diffusion tensor imaging. METHODS: Twenty one dyslexic children and 24 normal control children were recruited in the second and third grade of elementary school students. The fractional anisotropy (FA) values of 20 representative white matter tracts were estimated from the diffusion tensor imaging data of each subject using the Johns Hopkins University-white matter tractography atlas to determine the difference in white matter integrity between the dyslexic children and normal children. RESULTS: Compared to the normal control group, the FA values of the left inferior longitudinal fasciculus [F(1,39)=5.908, p<0.05] and temporal part of the right superior longitudinal fasciculus [F(1,39)=7.328, p=0.010] were significantly higher in the dyslexic group and there was no significant difference in the other tracts. CONCLUSION: In dyslexic children, compensatory pathways develop in the left inferior longitudinal fasciculus and in the temporal part of the right superior longitudinal fasciculus.