ABSTRACT
OBJECTIVES: The purpose of this study was to determine the association between serum lipid profiles and depression according to gender difference. METHODS: This retrospective cohort study included 27,452 subjects(15044 men and 12408 women) who underwent health examination. The duration was from January 2013 to December 2013. We estimate the correlation between serum lipid profile and Beck Depression Inventory(BDI) scores. We compare the effect size using beta coefficient. RESULTS: In men, serum Triglyceride level was correlated positively with BDI scores(r=0.020, p<0.01). Serum LDL-C and HDL-C were negatively correlated with BDI scores(r=-0.015, p<0.01 ; r=-0.016, p<0.05). In women, Triglyceride level was also correlated positively with BDI scores(r=0.020, p<0.01), Serum HDL-C were negatively correlated with BDI scores(r=-0.019, p<0.01). There was no statistical significance between Serum LDL-C and Beck Depression Inventory(BDI) score. CONCLUSIONS: Both men and women had more depressive symptoms when they had low serum HDL-C level or high serum Triglyceride level. The depression symptoms were more severe when serum LDL-C level was low only in men.
Subject(s)
Female , Humans , Male , Cholesterol , Cohort Studies , Depression , Retrospective Studies , TriglyceridesABSTRACT
Expression of zinc-finger protein 143 (ZNF143), a human homolog of the Xenopus transcriptional activator protein Staf, is induced by various DNA-damaging agents including etoposide, doxorubicin, and gamma-irradiation. ZNF143 binds to cisplatin-modified DNA, and its levels are increased in cancer cells that are resistant to anticancer drugs, including cisplatin, suggesting that it plays a role in carcinogenesis and cancer cell survival. However, the mechanism of ZNF143 induction in cancer cells remains unclear. Both insulin-like growth factor-1 (IGF-1) and its receptor (IGF-1R) have been reported to be overexpressed in cancer cells and to be related to anticancer drug resistance, but the identity of the relevant signaling mediators is still being investigated. In the present study, we observed that IGF-1 was able to induce ZNF143 expression in HCT116 human colon cancer cells and that wortmannin, an inhibitor of phosphatidylinositide 3-kinase (PI3-kinase), inhibited this induction, as did diphenyleneiodonium (DPI), an NADPH oxidase inhibitor, and monodansylcardavarine (MDC), a receptor internalization inhibitor. Treatment with MDC decreased the IGF-1-stimulated generation of reactive oxygen species. Taken together, these data suggest that IGF-1 induces ZNF143 expression in cancer cells via PI3-kinase and reactive oxygen species generation during receptor internalization.