- Serum Gamma-glutamyltransferase Levels and the Risks of Impaired Fasting Glucose in Healthy Men: A 2-year Follow-up.
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Joo Youn Shin, Jong Han Lim, Dai Ha Koh, Keun Sang Kwon, Yong Kyu Kim, Hwan Chul Kim, Yeui Cheol Lee, Ju Hyoung Lee, Moon Suk Nam, Sung Bin Hong, Shin Goo Park
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J Prev Med Public Health. 2006;39(4):353-358.
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 Abstract
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An increase in the serum gammaglutamyltransferase (GGT) concentration has been regarded as a marker of alcohol drinking or liver disease. Some reports, however, have suggested that the serum GGT may be a sensitive and early biomarker for the development of prediabetes and diabetes. In this study we investigated whether serum GGT is a reliable predictor of the incident impaired fasting glucose (IFG), including diabetes. METHODS: We performed a prospective study for two years (2002-2004). We analyzed the periodic health examination data from a total of 4,711 men. The examinations were done in the years 2002 and 2004. The analyzed data included a self-questionnaire, a physical examination and the laboratory results. Both IFG and diabetes were defined as a serum fasting glucose concentration of more than 100 mg/dL and 126 mg/dL, respectively. RESULTS: A total of 738 cases (15.7%) of incident IFG and 13 cases (0.3%) of diabetes occurred. The mean serum GGT concentrations were quite different between the normal (38.0 IU) and incident IFG groups (50.3 IU), and the incident diabetes group (66.0 IU) (p <0.001). After multivariable adjustment, the relative risks for incident IFG or diabetes across the baseline GGT categories (<10th, 10th-20th, 30th-40th, 50th-60th, 70th-80th and >90th percentile) were 1.0, 1.172 (0.769-1.785), 1.107 (0.725- 1.689), 1.444 (0.934-2.232), 2.061 (1.401-3.031) and 2.545 (1.784-3.631) (p-value for trend: <0.001). The risks significantly increased with increasing levels of GGT for 2 years; when comparing the increased groups (<10%, 10- 20%, >20%) versus the decreased over 20% group of GGT, the risks for IFG or diabetes were 1.334 (1.002-1.776), 1.613 (1.183-2.199) and 1.399 (1.092-1.794). CONCLUSIONS: Our findings suggest that serum GGT concentrations within its normal range may be an early predictor of the development of IFG and diabetes. As serum GGT is a relatively inexpensive test and a reliable marker, it might have important implications in public health promotion.
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Summary
- Mercuric Chloride Induces Apoptosis in MDCK Cells.
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Ju Hyoung Lee, Jung Ho Youm, Keun Sang Kwon
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J Prev Med Public Health. 2006;39(3):199-204.
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Abstract
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Mercury is a hazardous organ-specific environmental contaminant. It exists in a wide variety of physical and chemical states, each of which has unique characteristics for the target organ specificity. Exposure to mercury vapor and to organic mercury compounds specifically affects the CNS, while the kidney is the target organ for inorganic Hg compounds. METHODS: In this study, mercury chloride (HgCl2) was studied in a renal derived cell system, i.e., the tubular epithelial Madin-Darby canine kidney (MDCK) cell line, which has specific sensitivity to the toxic effect of mercury. MDCK cells were cultured for 6-24 hr in vitro in various concentrations (0.1-100 M) of HgCl2, and the markers of apoptosis or cell death were assayed, including DNA fragmentation, caspase-3 activity andwestern blotting of cytochrome c. The influence of the metal on cell proliferation and viability were evaluated by the conventional MTT test. RESULTS: The cell viability was decreased in a time and concentration dependent fashion: decreases were noted at 6, 12 and 24 hr after HgCl2 exposure. The increases of DNA fragmentation were also observed in the concentrations from 0.1 to 10 M of HgCl2 at 6 hr after exposure. However, we could not observe DNA fragmentation in the concentrations more than 25 M because the cells rapidly proceeded to necrotic cell death. The activation of caspase-3 was also observed at 6 hr exposure in the HgCl2 concentrations from 0.1 to 10 M. The release of cytochrome c from the mitocho-ndria into the cytosol, which is an initiator of the activation of the caspase cascade, was also observed in the HgCl2-treated MDCK cells. CONCLUSIONS: These results suggest that the activation of caspase-3 was involved in HgCl2-induced apoptosis. The release of cytochrome c from the mitochondria into the cytosol was also observed in the HgCl2-treated MDCK cells. These findings indicate that in MDCK cells, HgCl2 is a potent inducer of apoptosis via cytochrome c release from the mitochondria.
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