Jinkyung Cho

Randomized Controlled Trial of Training Intensity in Adiposity

The purpose of the study was to examine the effects of training intensity on abdominal fatness reduction and improvements of metabolic risk factors in Korean women (N=45, aged 45.4±7.3 yrs). Subjects were randomly assigned to control (CON, N=15) or low-intensity exercise (LIEX, N=15) or high-intensity exercise (HIEX, N=15). The LIEX and HIEX groups participated in a 12-wk exercise intervention at intensities of 40-50% and 70-75% of VO (2)max, respectively. Outcome assessments performed at baseline and at the end of 12-wk period included abdominal adipose tissues, VO (2)max, blood lipids, fasting glucose and insulin, and LPL- and HSL-mRNAs in abdominal subcutaneous adipose tissue (SAT). Unlike the CON group, women in the exercise groups had significant improvements in VO (2)max (+11%, P<0.001), SAT (-12%, P=0.026), TG (-23%, P=0.002), HDLC (+7.2%, P=0.013), insulin (-23%, P=0.037), and HOMA-IR (-25%, P=0.015) relative to baseline values. Changes in baseline CRF were in a dose-dependent manner based in intensity (-1.2±1.7, 2.1±2.8, and 4.7±3.2 ml/kg/min for CON, LIEX, and HIEX, respectively, P<0.001). We found no evidence that LIEX- and HIEX differ in their effects on abdominal adiposity, risk factors, and LPL- and HSL-mRNA expressions in SAT. In conclusion, the current findings suggest that low- and high-intensity exercise are equally effective in reducing abdominal adiposity and in improving risk factors.

Effect of Training Intensity on Nonalcoholic Fatty Liver Disease.

BACKGROUND Training intensity may play a key role in magnifying the protective effect of physical exercise against nonalcoholic fatty liver disease (NAFLD). PURPOSE This study aimed to test the hypothesis that vigorous-intensity and interval training is as effective as moderate-intensity and continuous exercise training on NAFLD in high-fat diet (HFD)-induced obese mice. METHODS C57BL/6 mice (N = 40) were fed a standard-chow diet (n = 10) or HFD (n = 30) for 16 wk. After the initial 8-wk dietary treatments, HFD mice were further divided into HFD only (n = 10), HFD plus vigorous-intensity and interval treadmill running (VIT) (n = 10), and HFD plus moderate-intensity and continuous treadmill running (MIT) (n = 10) for the remaining 8-wk period. RESULTS Chronic exposure to HFD resulted in hepatic steatosis in conjunction with an obese and impaired glucose tolerance condition characterized by dyslipidemia, hyperinsulinemia elevated markers for the liver damage, and hypoadiponectinemia. Although VIT and MIT alleviated the NAFLD conditions, the former was more effective at alleviating hepatic steatosis than the latter. The intensity-dependent benefit of exercise training against hepatic steatosis was associated with greater activation of VIT on hepatic AMP-mediated protein kinase in conjunction with greater suppressive effect of VIT on hypoadiponectinemia, downregulation of the Adiponectin receptor 2 signaling pathway, and upregulation of the NF-κB signaling pathway in the liver. CONCLUSIONS The current findings suggest that VIT is an alternative way of exercise training to combat hepatic steatosis associated with an obese and impaired glucose tolerance phenotype.

Effect of aerobic exercise training on non-alcoholic fatty liver disease induced by a high fat diet in C57BL/6 mice

[Purpose] The aim of this study was to investigate the effects of aerobic exercise training on a high fat diet (HFD)-induced fatty liver and its metabolic complications in C57BL/6 mice. [Methods] Mice at 5-month old (n = 30) were randomly assigned to standard chow (SC + CON, n = 10) and high-fat diet (HFD, n = 20), and they were subjected to SC and HFD, respectively, for 23-week. After 15-week of HFD, mice in the HFD group were further assigned to HFD (HFD + CON, n = 10) or exercise training (HFD + EX, n = 10) groups. The HFD + EX mice were subjected to aerobic treadmill running during the last 8-week of the 23-week HFD course. Outcomes included hepatic steatosis, insulin resistance, and expression of genes involved in mitochondrial function and/or fatty oxidation as well as de novo lipogenesis and/or triacylglycerol (TAG) synthesis. [Results] Treadmill running ameliorated impaired glucose tolerance and insulin resistance secondary to the HFD. The beneficial effects of treadmill running were associated with enhanced molecular markers of mitochondrial function and/or fatty acids oxidation (i.e., PPARα and CPT1a mRNAs, pAMPK/AMPK, pACC, and SIRT1 protein) as well as suppressed expression of de novo lipogenesis and/or TAG synthesis (i.e., SREBP1c, lipin1 and FAS mRNAs) in the liver. [Conclusion] The current findings suggest that aerobic exercise training is an effective and non-pharmacological means to combat fatty liver and its metabolic complications in HFD-induced obese mice.

Treadmill Running Reverses Cognitive Declines due to Alzheimer Disease.

PURPOSE This study investigated the effect of treadmill running on cognitive declines in the early and advanced stages of Alzheimer disease (AD) in 3xTg-AD mice. METHODS At 4 months of age, 3xTg-AD mice (N = 24) were assigned to control (AD + CON, n = 12) or exercise (AD + EX, n = 12) group. At 24 months of age, 3xTg-AD mice (N = 16) were assigned to AD + CON (n = 8) or AD + EX (n = 8) group. The AD + EX mice were subjected to treadmill running for 12 wk. At each pathological stage, the background strain mice were included as wild-type control (WT + CON, n = 8-12). RESULTS At the early stage of AD, 3xTg-AD mice had impaired short- and long-term memory based on Morris water maze along with higher cortical Aβ deposition, higher hippocampal and cortical tau pathology, and lower hippocampal and cortical PSD-95 and synaptophysin. A 12-wk treadmill running reversed the impaired cognitive declines and significantly improved the tau pathology along with suppression of the decreased PSD-95 and synaptophysin in the hippocampus and cortex. At the advanced stage of AD, 3xTg-AD mice had impaired short- and long-term memory along with higher levels of Aβ deposition, soluble Aβ1-40 and Aβ1-42, tau pathology, and lower levels of brain-derived neurotrophic factor, PSD-95, and synaptophysin in the hippocampus and cortex. A 12-wk treadmill running reversed the impaired cognitive declines and significantly improved the Aβ and tau pathology along with suppression of the decreased synaptic proteins and brain-derived neurotrophic factor in the hippocampus and cortex. CONCLUSIONS The current findings suggest that treadmill running provides a nonpharmacological means to combat cognitive declines due to AD pathology.

Serum Vitamin D, Physical Activity, and Metabolic Risk Factors in Korean Children.

PURPOSE The purpose of this study was to investigate the relationship of serum vitamin D levels with lifestyle factors, including body fatness and physical activity (PA) parameters, and the clustering of metabolic risk factors in the Korean pediatric population. METHODS Serum 25-hydroxyvitamin D levels, accelerometer-based PA, and body fatness and metabolic syndrome parameters were assessed in a sample of children of Korean descent (N = 310). Correlation and multivariate linear regression were used to explore the relationships among serum vitamin D levels, lifestyle factors, and the clustering of metabolic risk factors in the study sample. RESULTS Serum vitamin D levels were negatively associated with body fatness parameters, including body mass index, percent body fat, and waist circumference, but positively associated with accelerometer-based PA including low, moderate, and vigorous levels. In addition, serum vitamin D levels were inversely related to total cholesterol, triglycerides, fasting glucose, and insulin. A stepwise linear regression model showed that both low serum vitamin D levels and decreased vigorous PA were independent predictors for individual variation in the clustering of metabolic risk factors in this study sample. CONCLUSION The results of this study suggest that an increase in vigorous PA and vitamin D intake should be two major targets of public health inventions against the clustering of metabolic risk factors in the Korean pediatric population.

Relationship of PGC-1α Gene Polymorphism With Insulin Resistance Syndrome in Korean Children:

This study aimed to investigate the associations between peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) gene Gly482Ser polymorphism (rs8192678) and parameters of insulin resistance in a sample of Korean children. A total of 286 children aged 10 to 12 years old were recruited from local elementary schools. Measured variables included body fat, blood pressures, blood lipids, glucose, insulin, homeostasis model assessment of insulin resistance (HOMA-IR), and accelerometer-based physical activity (PA). Significant differences in percentage body fat (P = .016), insulin (P = .013), and HOMA-IR (P = .007) were found according to Gly482Ser genotype, with no significant genotype differences in the other measured variables. The genotype-specific differences in insulin (P = .136) and HOMA-IR (P = .067) were significantly attenuated when adjusted for age, sex, Tanner stage, body fat, and PA. The findings of the study suggest that the genetic effects of the PGC-1α genotypes on parameters of insulin resistance might be modulated by lifestyle factors, including PA and body fatness.

Association between serum vitamin D status and metabolic syndrome in Korean young men.

PURPOSE This study examined the relations of serum vitamin D levels to body fatness, cardiorespiratory fitness (CRF), and metabolic risk factors in young adults in Korea. METHODS Between 2007 and 2009, 799 young men completed a health examination. Body fatness, CRF based on a maximal treadmill exercise test, and measurements of metabolic risk factors were measured in study participants. Participants were classified by serum vitamin D levels as deficient (<12.5 ng·mL), insufficient (≥12.5 to <20 ng·mL), and sufficient (>20 ng·mL) and by CRF as unfit (lowest 20%) and fit (remaining 80%) based on age-standardized distribution of V˙O2max values in this study population. Body fatness, CRF, and metabolic risk factors were evaluated according to serum vitamin D classification. A clustered metabolic risk score was computed by summing standardized scores for waist circumference, resting blood pressures, triacylglycerols, the inverse of high-density lipoprotein cholesterol, glucose, and insulin. RESULTS Linear decreases in body fatness and metabolic risk factors were observed, as was a linear increase for CRF across incremental vitamin D categories. A linear decrease was found in the clustered metabolic risk score across incremental vitamin D categories. Compared to the fit group (reference), the unfit group had significantly higher risks for serum vitamin D inadequacy before and after adjusting for age, smoking, and body fatness parameters. CONCLUSIONS The findings of the study suggest that increasing vitamin D intake, eating a healthy diet, and getting enough outdoor physical activity should be promoted as nonpharmacologic means to improve CRF and prevent a clustering of metabolic risk factors in young adults.

GNB3 C825T Polymorphism and Elevated Blood Pressure

Unlike in Europeans and Africans, the relationship between the human guanine nucleotide binding beta polypeptide 3 (GNB3) C825T gene polymorphism (rs5443) and blood pressures is inconsistent in Asians. The aim of the study was to investigate whether the GNB3 genotype demonstrates different associations with resting blood pressure and body fatness across cardio/respiratory fitness (CRF) levels. A total of 727 Korean women aged 31-60 years (mean, 47.8+/-5.4 years) participated in the study. In subgroup analyses of the obese group, TT individuals had significantly higher values of body weight than CC and CT individuals (p=0.006 and p=0.006, respectively) and body mass index (BMI) (p=0.002 and p=0.011, respectively). TT and CT individuals also tended to have higher CRF values than CC individuals. Regression analyses showed that the association between GNB3 genotype and resting blood pressure remained significant after adjustment for age and menopause, but was not significant after additional adjustment for body fatness. In summary, the findings of this study suggest that body fatness and CRF might modify the GNB3-mediated genetic susceptibility to elevated resting blood pressures in middle-aged Korean women.

ACTN3 Gene and Susceptibility to Sarcopenia and Osteoporotic Status in Older Korean Adults

Background Little information is available about molecular markers for sarcopenia and osteoporosis in Asian populations. Objective This study investigated the association of the ACTN3 polymorphism with sarcopenia and osteoporotic status in older Korean adults. Methods Older Korean 62 men and 270 women (mean age 73.7 ± 6.6 years) participated in this study. Body mass index, percent body fatness, appendicular skeletal muscle mass, and bone mineral density of the lumbar spine, femur, and total body were analyzed with dual-energy X-ray absorptiometry. ACTN3 R/X genotyping was determined using TaqMan probes. Results Determination of odds ratios (ORs) and 95% confidence intervals (CIs) using binary logistic regression analyses showed that XX homozygotes were at a significantly higher risk of sarcopenia (OR = 2.056, 95%  CI = 1.024–4.127, p = 0.043) and osteoporosis (OR = 2.794, 95%  CI = 1.208–5.461, p = 0.016) than RR homozygotes (reference group, OR = 1). The OR of XX homozygotes for having sarcopenia remained significant (OR = 2.237, 95%  CI = 1.044–4.836, p = 0.038) after adjustments for age, gender, body fatness, and serum vitamin D. The OR of XX homozygotes for having osteoporosis was no longer significant (OR = 2.682, 95%  CI = 0.960–7.942, p = 0.075) after adjustments for the covariates. Conclusion Our findings suggest that the ACTN3 R577X genotype may influence decline in muscle and bone health phenotypes in older Korean adults.

Exercise Training Improves Whole Body Insulin Resistance via Adiponectin Receptor 1.

Little is known regarding whether adiponectin receptors mediate high-intensity interval training (HIT)-induced improvement of insulin resistance associated with obesity. This study investigated the effect of HIT on whole body insulin resistance in high-fat diet-induced obese mice. 5-week-old male mice (N=30) were randomly assigned to standard chow (SC) (n=10) or HFD (n=20) for 23 weeks. After 15 weeks of dietary treatment, the HFD mice were further assigned to HFD (n=10) or HFD plus HIT (HFD+HIT, n=10). The HFD+HIT mice were subjected to HIT during the last 8 weeks of the 23-week HFD course. HFD resulted in whole body insulin resistance, hypoadiponectinemia, suppressed expression of adiponectin receptor 1(AdipoR1) and 2 (AdipoR2), suppressed expression of phosphorylated AMP-activated protein kinase (p-AMPK) and NAD-dependent deacetylase sirtuin-1 (SIRT1), and decreased mRNAs of peroxisome proliferator-activated receptor-α (PPARα), carnitine palmitoyltransferase I (CPT1), and acyl CoA oxidase (ACO) in skeletal muscle. In contrast, HIT alleviated whole body insulin resistance and prevented decreased levels of total adiponectin in both serum and adipose tissue. HIT also prevented the down-regulation of AdipoR1 and AMPK/SIRT1 proteins and the down-regulation of PPARα, CPT1, and ACO mRNAs. The current findings show that HIT alleviates whole body insulin resistance due to HFD-induced obesity via the AdipoR1 and AMPK/SIRT1 mediated-signaling pathway in skeletal muscle, implying the potential role of HIT to combat this metabolic condition.