Relationship between metabolic syndrome and metabolic syndrome score with ß-cell function by gender in non-diabetic Korean populations.

Aims: The present study was conducted to assess the association of metabolic syndrome (MetS) and the MetS score (MSS) with ß-cell function by gender in Korean non-diabetic populations. Methods: This study used the data from the 2015 Korean National Health and Nutrition Examination Survey including 4380 adults, aged 20 or older. Results: After adjusting for related variables (with exception of body mass index [BMI]), MetS (p < 0.001) and MSS (p < 0.001) were positively associated with homeostasis model assessment of ß-cell function (HOMA-B), in both men and women. When further adjusting for BMI, MetS (p = 0.002) and MSS (p = 0.006) were positively associated with HOMA-B in women, whereas the association of MetS (p = 0.140) or MSS (p = 0.697) and HOMA-B was no longer significant in men. Conclusion: MetS and MSS increases were positively associated with ß-cell function in non-diabetic Korean women, but not in non-diabetic Korean men.

The Relationship Between the Metabolic Syndrome and Systolic Inter-Arm Systolic Blood Pressure Difference in Korean Adults.

BACKGROUND: The present study was conducted to assess the relationship between metabolic syndrome and systolic inter-arm blood pressure difference (sIAD) in Korean adults. METHODS: This study included 410 adults (235 males, 175 females) who were over 30 years old and had undergone a health check from July to December in 2013. RESULTS: The incidence of high sIAD and metabolic syndrome were 23.4% and 23.2%, respectively. Key study results were as follows: First, the sIAD levels increased significantly with an increase in metabolic syndrome score (p<0.001), shown by sIAD levels after adjusted the variables that affect sIAD levels (age, gender, smoking, drinking, exercising, total cholesterol, and body mass index). These were 4.6±0.7 mmHg for metabolic syndrome score (MSS) 0; 5.8±0.5 mmHg for MSS 1; 6.2±0.6 mmHg for MSS 2, 9.2±0.8 mmHg for MSS 3; and 9.9±1.2 mmHg for MSS ≥4 (p<0.001). Second, the sIAD level of the metabolic syndrome group (9.3±0.7 mmHg) was significantly higher (p<0.001) than for the nonmetabolic syndrome group (5.7±0.3 mmHg). CONCLUSIONS: In conclusion, metabolic syndrome and an increased number of its components are associated with the sIAD levels in Korean adults.

Emodin attenuates radioresistance induced by hypoxia in HepG2 cells via the enhancement of PARP1 cleavage and inhibition of JMJD2B.

Radioresistance in the tumor and radiotoxicity in the non­tumorous liver significantly restrict efficient radiotherapy of hepatocellular carcinoma (HCC). It is therefore important to study the radioresistance mechanism and development of radiosensitization to optimize the effect of irradiation on cancer cells. Emodin (1, 3, 8­trihydroxy­6­methylanthraquinone) is a plant­derived polyphenol, possessing anticancer properties. It is known to act as a radiosensitizer in human HCC cell lines. The aim of this study was to evaluate the role of emodin in radioresistance of human HCC cell lines as well as the underlying radiosensitization mechanism. The human HCC cell line (HepG2) was used in this study. Four different treatment groups, i.e., no treatment (control), irradiation (10 Gy, one fraction), emodin (10 µM), and a combination of irradiation and emodin (10 Gy+10 µM) were used for two environmental conditions: hypoxia (1% O2) and normoxia (20% O2). The cells were exposed to the respective treatments for 24 and 72 h. Following the treatment, the cell viability was determined by the 3­(4,5­dimethylthiazol­2­yl)­2,5­diphenyltetrazolium bromide (MTT) assay, and the radiosensitization mechanism was evaluated by western blotting. The proliferation of HepG2 cells was significantly suppressed in the treatment groups under hypoxic and normoxic conditions in the following order: combination of irradiation and emodin>irradiation only >emodin only. The combination of irradiation and emodin induced apoptotic signaling activities such as cleavage of poly (ADP­ribose) polymerase (PARP)­1 as well as the downregulation of epigenetic signaling such as JMJD1A and JMJD2B. Emodin attenuated radioresistance in the HepG2 cells via upregulation of the apoptotic signals and down-regulation of the proliferative signals. These results suggested that emodin is a potential candidate for the radiosensitization of HCC cells and can aid in identifying novel therapeutic strategies for HCC radiotherapy.