2006 Vol. 19, No. 1
Report on Childhood Obesity in China (2)Verification of BMI Classification Reference for Overweight and Obesity in Chinese Children and Adolescents
2006, 19(1): 1-7.
Objective To verify Working Group for Obesity in China (WGOC) recommended body mass index (BMI) classification reference for overweight and obesity in Chinese children and adolescents using the data of 2002 China Nationwide Nutrition and Health Survey. Methods Pediatric metabolic syndrome (MetS) and abnormality of each risk factor for MetS were defined using the criteria for US adolescents. Definition of hyper-TC, LDL, and dyslipidemia in adults was applied as well. The average level and abnormality rate of the metabolic indicators were described by BMI percentiles and compared with general linear model analysis. Receiver operating characteristic analysis was used to summarize the potential of BMI to discriminate between thepresence and absence of the abnormality of these indicators. Results There was neither significantly increasing nor significantly decreasing trend of biochemical parameter levels in low BMI percentile range (＜65th). Slight increasing trend from the 75th and a significant increase were found when BMI≥85th percentile. In general, the prevalence of the examined risk factors varied slightly when BMI percentile＜75th, and substantial increases were consistently seen when BMI percentile≥75th. As an indicator of hyper-TG, hypertension and MetS, the sensitivity and specificity were equal at the point of BMI＜75th percentile, and the Youden's index of risk factors also reached peak point before 75th percentile except for MetS. When the BMI percentile was used as the screening indicator of MetS, Youden's index reached peak point at 85th percentile, just the point in the ROC graph that was nearest to the upper left corner. Conclusion The BMI classification reference for overweight and obesity recommended by WGOC is rational to predict and prevent health risks in Chinese children and adolescents. Lower screening cut-off points, such as 83th percentile or 80th percentile, should not be excluded when they are considered as overweight criteria in future intervention or prevention studies.
2006, 19(1): 8-14.
Objective To investgate the metabolism of terephthalic acid (TPA) in rats and its mechanism. Methods Metabolism was evaluated by incubating sodium terephthalate (NaTPA) with rat normal liver microsomes, or with microsomes pretreated by phenobarbital sodium, or with 3-methycholanthrene, or with diet control following a NADPH-generating system. The determination was performed by high performance liquid chromatography (HPLC), and the mutagenic activation was analyzed by umu tester strain Salmonella typhimurium NM2009. Expression of CYP4B 1 mRNA was detected by RT-PCR. Results The amount of NaTPA (12.5-200 μmol· L-1) detected by HPLC did not decrease in microsomes induced by NADPH-generating system. Incubation of TPA (0.025-0.1 mmol·L-1) with induced or noninduced liver microsomes in an NM2009 umu response system did not show any mutagenic activation. TPA exposure increased the expression of CYP4B 1 mRNA in rat liver, kidney, and bladder. Conclusion Lack of metabolism of TPA in liver and negative genotoxic data from NM2009 study are consistent with other previous short-term tests, suggesting that the carcinogenesis in TPA feeding animals is not directly interfered with TPA itself and/or its metabolites.
2006, 19(1): 15-20.
Objective To observe the effects of fenvalerate on calcium homeostasis in rat ovary. Methods Female SpragueDawley rats were orally given fenvalerate at daily doses of 0.00, 1.91, 9.55, and 31.80 mg/kg for four weeks. The ovary ultrastucture was observed by electron microscopy. Serum free calcium concentration was measured by atomic absorption spectrophotometry. The activities of phosphorylase a in rat ovary were evaluated by the chromatometry. The total content of calmodulin in ovary was estimated by ELISA at each stage of estrous cycle. Radioimmunoassay (RIA) was used to evaluate the level of serum progesterone. Results Histopathologically, damages of ovarian corpus luteum cells were observed. An increase in serum free calcium concentration was observed in rats treated with 31.80mg/kg fenvalerate. The activities of phosphorylase a enhanced in all treated groups, and fenvalerate increased the total content of calmodulin significantly in estrus period. Serum progesterone levels declined in fenvalerate exposed rats in diestrus. Conclusion Fenvalerate interferes with calcium homeostasis in rat ovary. Also, the inhibitory effects of fenvalerate on serum progesterone levels may be mediated partly through calcium signals.
2006, 19(1): 21-26.
Objective The toxicology of TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin) has been studied mainly with regard to the carcinogenicity of its metabolites, but its phototoxicity is not well understood. Although some studies have indicated the lethal phototoxicity of TCDD, this study was designed to investigate its effect on SPC-A1 cells. Methods SPC-A1 cells were cultured in 1640 medium and treated with 10 nmol/L, 0.1 μmol/L, 1 μmol/L TCDD for either 24 h or 96 h at each concentration. SPC-A1 cells were co-cultured with TCDD at different concentrations. Then the cell morphology, DNA fragment electrophoresis, and cell cycle were analyzed by flow cytometry, and enzyme assays were used to observe the effect of TCDDon the morphology, growth rate, and enxyme change of SPC-A1 cells. Results With the increasing concentrations of TCDD and prolongation of culture time, the morphology of SPC-A1 cells was changed from round shape to spindle, and the ability of SPC-A1 cells to adhere to wall was decreased. With debris emitted around the cells, the morphologic changes included reduction in cell volume. Nuclear chromatin condensation and PI were observed. With the increasing concentrations of TCDD,DNA ladder occurred. After treatment with TCDD, extraction of cancer cells exhibited typical DNA fragmentation, and flow cytometry analysis showed apoptosis in a dose-dependent manner. As the concentration of TCDD rose from 10 nmol/L to 1 μmol/L, the ratio of apoptotic cells increased from 10.76% to 21.82%. Conclusions TCDD has in vitro cytotoxicity on SPC-A1 cells, and the cytotoxicity is positively related to its concentration and culture time. TCDD may inhibit the growth and proliferation of SPC-A 1 cells through the pathway of apoptosis introduction.