Association between Dyslipidemia and the Prevalence of Colon Polyps Based on a Health Evaluation of Subjects at a Hospital.

BACKGROUND: Colonic neoplasm is associated with western diet intake and physical inactivity. These life styles are also risk factors for dyslipidemia and metabolic syndrome. The aim of this study was to evaluate the association between dyslipidemia and the prevalence of colon polyps including colon adenoma as a precancerous lesion of colonic neoplasms. METHODS: We selected subjects undergoing a colonoscopy for health screening at the Health Promotion Center of Eulji General Hospital from January 2006 to June 2010. Subjects with histories of cancers, dyslipidemia treatment, and other intestinal diseases like Crohn's disease and ulcerative colitis were excluded. The total numbers of subjects included in the study was 605. Chi-square test and t-test and were used for the analysis. Additionally we used multivariate logistic regression to adjust for sex, age, smoking, drinking, and other risk factors. RESULTS: The prevalence of colon polyps was 48.70% and 28.05% in males and females, respectively. When adjusting for variables that included age, body mass index, hypertension, diabetes mellitus, smoking, drinking, and exercise, dyslipidemia was not significantly associated with the prevalence of colon polyps. However upon analyzing adenomatous colon polyps in men, dyslipidemias due to triglycerides and high density lipoproteins were significant factors (odds ratio [OR], 2.13; confidence interval [CI], 1.14 to 3.98; OR, 2.24; CI, 1.15 to 4.34, respectively). CONCLUSION: Dyslipidemia was not a significant factor in the prevalence of colon polyps. However it had a significant association with the prevalence of adenomatous colon polyps in men.

The Relationship between Metabolic Syndrome and Pulmonary Function.

BACKGROUND: Impaired lung function is associated with mortality rate from cardiovascular and all other death causes. There were previous studies on the relationship between lung function impairment and metabolic syndrome, but they are insufficient. This study was conducted on Koreans to analyze each component of metabolic syndrome as well as its variability between sexes. METHODS: 1,370 subjects underwent a health examination at the Eulji General Hospital Health Center. We examined the association between lung function measurement (forced expiratory volume for 1 second [FEV(1)], forced vital capacity [FVC], FEV(1)/FVC) and metabolic syndrome using Student t-test, Pearson partial correlation coefficient, and analysis of covariance for statistical analysis, and we adopted metabolic syndrome defined by American Heart Association/National Heart, Lung, and Blood Institute in Asia. RESULTS: Men with metabolic syndrome tended to experience lung function impairment. In terms of association to each metabolic syndrome component, metabolic syndrome components in men were associated with pulmonary function impairment and the more metabolic syndrome diagnostic criteria factors the patients had, the more severe their pulmonary function tended to decline. In women, waist circumference, triglyceride and high-density lipoprotein cholesterol were associated with pulmonary function change. CONCLUSION: In men, all metabolic syndrome components were associated with pulmonary function impairment, and the more metabolic syndrome components men had, the more severe their pulmonary functions decline. In women, components of metabolic syndrome were not associated with pulmonary function impairment.

Involvement of AMP-activated protein kinase and p38 mitogen-activated protein kinase in 8-Cl-cAMP-induced growth inhibition.

8-Cl-cAMP (8-chloro-cyclic AMP), which induces differentiation, growth inhibition and apoptosis in various cancer cells, has been investigated as a putative anti-cancer drug. Although we reported that 8-Cl-cAMP induces growth inhibition via p38 mitogen-activated protein kinase (MAPK) and a metabolite of 8-Cl-cAMP, 8-Cl-adenosine mediates this process, the action mechanism of 8-Cl-cAMP is still uncertain. In this study, it was found that 8-Cl-cAMP-induced growth inhibition is mediated by AMP-activated protein kinase (AMPK). 8-Cl-cAMP was shown to activate AMPK, which was also dependent on the metabolic degradation of 8-Cl-cAMP. A potent agonist of AMPK, 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR) could also induce growth inhibition and apoptosis. To further delineate the role of AMPK in 8-Cl-cAMP-induced growth inhibition and apoptosis, we used two approaches: pharmacological inhibition of the enzyme with compound C and expression of a dominant negative mutant (a kinase-dead form of AMPKalpha2, KD-AMPK). AICAR was able to activate p38 MAPK and pre-treatment with AMPK inhibitor or expression of KD-AMPK blocked this p38 MAPK activation. Cell growth inhibition was also attenuated. Furthermore, p38 MAPK inhibitor attenuated 8-Cl-cAMP- or AICAR-induced growth inhibition but had no effect on AMPK activation. These results demonstrate that 8-Cl-cAMP induced growth inhibition through AMPK activation and p38 MAPK acts downstream of AMPK in this signaling pathway.

Rap1 and p38 MAPK mediate 8-chloro-cAMP-induced growth inhibition in mouse fibroblast DT cells.

8-Cl-cAMP, which is known to induce differentiation, growth inhibition, and apoptosis in various cancer cells, has been investigated as a putative anti-cancer drug. Previously, we reported that 8-Cl-cAMP and its metabolite 8-Cl-adenosine induce growth inhibition and apoptosis through p38 mitogen-activated protein kinase (MAPK) activation. To further investigate the signal mechanisms that regulate the cellular effects of 8-Cl-cAMP, we focused on a small GTPase Rap1 that is known to be involved in growth inhibition and reverse-transformation. 8-Cl-cAMP and 8-Cl-adenosine could increase Rap1 activity, which was blocked by ABT702-an adenosine kinase inhibitor. This suggests that 8-Cl-cAMP-induced Rap1 activation is also dependent on the metabolic degradation of 8-Cl-cAMP. Overexpression of a constitutively active mutant form of Rap1 (Rap1V12) attenuated cellular growth and soft-agar colony formation, which was basically the same effect as that observed with the 8-Cl-cAMP treatment. Furthermore, the Rap1V12 transfectant showed a high level of p38 MAPK activation. However, 8-Cl-cAMP-induced Rap1 activation was not diminished by SB203580, a p38 MAPK inhibitor, suggesting that Rap1 activation might act upstream of p38 MAPK activation during 8-Cl-cAMP-induced growth inhibition.