The Prevalence of Obesity and Metabolic Syndrome in the Korean Military Compared with the General Population.

BACKGROUND: Obesity and related metabolic disorders are growing health challenges worldwide and individuals at military service are not exceptions. The purpose of this study was to examine the prevalence of obesity and metabolic syndrome (MS) in the Korean military and to compare with the general population. METHODS: This was a cross-sectional study of 4,803 young military participants who underwent a corporal health-screening program between October 2013 and October 2014. The National Cholesterol Education Program Adult Treatment Panel III criteria was used to identify MS. We also sampled 1,108 men aged 19-29 years from the Korea National Health and Nutritional Examination Survey from 2010 to 2013 to compare with their military counterparts. RESULTS: The mean age of military participants was 20.8 ± 1.1 years, and 20.6% (n = 988) were obese. The prevalence of MS was 0.8% in military participants, while 7.9% in general population. The risk factors of MS were less prominent among military participants relative to civilians, with the exception of high blood pressure, of which prevalence was higher among military participants (21.5% vs. 18.2%, respectively). In multiple logistic analysis, high physical activity conferred lower odds of MS and obesity in military participants (odds ratios, 0.19 and 0.81, respectively). Age older than 25 years increased risk of most components of MS among civilians. CONCLUSION: The prevalence of obesity and MS is lower in military participants compared with civilians of similar age. Monitoring of high blood pressure and proper stress management are warranted in those at military service.

Trichostatin A resistance is facilitated by HIF-1α acetylation in HeLa human cervical cancer cells under normoxic conditions.

Trichostatin A (TSA) is an anticancer drug that inhibits histone deacetylases (HDACs). Hypoxia-inducible factor 1 (HIF-1) participates in tumor angiogenesis by upregulating target genes, such as vascular endothelial growth factor (VEGF). In the present study, we investigated whether TSA treatment increases HIF-1α stabilization via acetylation under normoxic conditions, which would lead to VEGF upregulation and resistance to anticancer drugs. TSA enhanced total HIF-1α and VEGF-HRE reporter activity under normoxic conditions. When cells were transfected with GFP-HIF-1α, treatment with TSA increased the number of green fluorescence protein (GFP)-positive cells. TSA also enhanced the nuclear translocation of HIF-1α protein, as assessed by immunoblotting and as evidenced by increased nuclear localization of GFP-HIF-1α. An increase in the interaction between HIF-1α and the VEGF promoter, which was assessed by a chromatin immunoprecipitation (ChIP) assay, led to activation of the VEGF promoter. TSA acetylated HIF-1α at lysine (K) 674, which led to an increase in TSA-induced VEGF-HRE reporter activity. In addition, TSA-mediated cell death was reduced by the overexpression of HIF-1α but it was rescued by transfection with a HIF-1α mutant (K674R). These data demonstrate that HIF-1α may be stabilized and translocated into the nucleus for the activation of VEGF promoter by TSA-mediated acetylation at K674 under normoxic conditions. These findings suggest that HIF-1α acetylation may lead to resistance to anticancer therapeutics, such as HDAC inhibitors, including TSA.

Dynamic rearrangement of F-actin is required to maintain the antitumor effect of trichostatin A.

Actin plays a role in various processes in eukaryotic cells, including cell growth and death. We investigated whether the antitumor effect of trichostatin A (TSA) is associated with the dynamic rearrangement of F-actin. TSA is an antitumor drug that induces hyper-acetylation of histones by inhibiting histone deacetylase. HeLa human cervical cancer cells were used to measure the antitumor effect of TSA. The percent cell survival was determined by an MTT assay. Hypodiploid cell formation was assessed by flow cytometry. Collapse of the mitochondrial membrane potential (MMP) was identified by a decrease in the percentage of cells with red MitoProbe J-aggregate (JC-1) fluorescence. Cell survival was reduced by treatment with TSA, as judged by an MTT assay and staining with propidium iodide, FITC-labeled annexin V, or 4',6-diamidino-2-phenylindole (DAPI). TSA also induced an MMP collapse, as judged by the measurement of intracellular red JC-1 fluorescence. In addition, the F-actin depolymerizers cytochalasin D (CytoD) and latrunculin B (LatB) induced an MMP collapse and increased apoptotic cell death in HeLa cells. However, our data show that apoptotic cell death and the MMP collapse induced by TSA were decreased by the co-treatment of cells with CytoD and LatB. These findings demonstrate that the dynamic rearrangement of F-actin might be necessary for TSA-induced HeLa cell apoptosis involving a TSA-induced MMP collapse. They also suggest that actin cytoskeleton dynamics play an important role in maintaining the therapeutic effects of antitumor agents in tumor cells. They further suggest that maintaining the MMP could be a novel strategy for increasing drug sensitivity in TSA-treated tumors.