Purpose: The main purpose of this study was to examine the relationship between sedentary time and metabolic syndrome. Association of accelerometer and self-reported sedentary time on metabolic syndrome were also compared. Methods: A total of 1,354 adults (men, 492; women, 862), aged 19 to 65 years, who wore the accelerometer from the Korea National Health and Nutrition Examination Survey were included in the analysis. Four subgroups were created based on quartiles of daily sedentary time for analytical purposes. Metabolic syndrome was defined according to the International Diabetes Federation. Logistic regression was used to predict the odds ratio (OR), and 95% confidence interval (CI) of the relationship between sedentary time and metabolic syndrome after adjusting for sex, age, education level, family income, smoking, alcohol consumption, body mass index, and accelerometer wear time. Results: Accelerometer measured sedentary time displayed stronger associations with the metabolic syndrome than did self-reported sedentary time. When controlling for covariates, participants in the fourth quartile of the accelerometer measured sedentary time predicted the highest odds of having metabolic syndrome (OR, 1.99; 95% CI, 1.18– 3.34). However, participants in the second quartile only of self-reported sedentary time predicted the odds of having metabolic syndrome (OR, 1.60; 95% CI, 1.01– 2.52). Conclusion Sedentary time was related to metabolic syndrome. This relationship tended to be more consistent and stronger for accelerometer measured sedentary time than for self-report. Current results suggest that reducing daily sedentary time may help prevent metabolic syndrome.

Intellectual disability (ID) is a neurodevelopmental disorder defined by below-average intelligence (intelligence quotient of <70) accompanied by adaptive behavior deficits. Defects in the functions of neural stem cells during brain development are closely linked to the pathogenesis of ID. To understand the molecular etiology of ID, we examined neural stem cells from individuals with Duchenne muscular dystrophy (DMD), a genetic disorder in which approximately one-third of the patients exhibit ID. In this study, we generated induced pluripotent stem cells from peripheral blood mononuclear cells from a normal individual and DMD patients with and without ID to identify ID-specific functional and molecular abnormalities. We found defects in neural ectoderm formation in the group of DMD patients with ID. Our transcriptome analysis of patient-derived neural stem cells revealed altered expression of genes related to the hippo signaling pathway and neuroactive ligand-receptor interaction, implicating these in the pathogenesis of ID in patients with DMD.

Intellectual disability (ID) is a neurodevelopmental disorder defined by below-average intelligence (intelligence quotient of <70) accompanied by adaptive behavior deficits. Defects in the functions of neural stem cells during brain development are closely linked to the pathogenesis of ID. To understand the molecular etiology of ID, we examined neural stem cells from individuals with Duchenne muscular dystrophy (DMD), a genetic disorder in which approximately one-third of the patients exhibit ID. In this study, we generated induced pluripotent stem cells from peripheral blood mononuclear cells from a normal individual and DMD patients with and without ID to identify ID-specific functional and molecular abnormalities. We found defects in neural ectoderm formation in the group of DMD patients with ID. Our transcriptome analysis of patient-derived neural stem cells revealed altered expression of genes related to the hippo signaling pathway and neuroactive ligand-receptor interaction, implicating these in the pathogenesis of ID in patients with DMD.