The aim of this work was to establish the prevalence of overweight and obesity and its associated comorbidities in a Chinese population older than 20 years of age. A group of 2776 randomly selected adults (20-94 years of age) living in the Huayang Community in Shanghai, China, were investigated between 1998 and 2000. Body weight, height, waist and hip circumferences and blood pressure were measured, as were fasting blood glucose, fasting insulin and lipid profile, as well as blood glucose 2 h after a glucose load, and a 75-g glucose tolerance test was performed. The prevalence of overweight was 29.5% and obesity was 4.3%, with a greater number of women being obese than men. More than one-third of the population had abnormal lipid levels. Impaired glucose regulation (IGR) occurred in 10.8%; and 9.8% of the population were classified as having type 2 diabetes mellitus. Hypertension was present in 58.4% of this population. About 21% and 29.3% of the population suffered from high total cholesterol and high triglyceride, respectively. The prevalence of metabolic syndrome was 10.2%. The prevalence of diabetes, IGR and metabolic syndrome increased progressively in association with a body mass index (BMI) of >23 kg m(-2). Hence, although the prevalence of obesity is low in this Chinese population, higher BMI and waist circumference values are clearly associated with an increasing prevalence of comorbidities. The absolute risk of having diabetes, IGR and metabolic syndrome is high in adults with a BMI of > or =23 kg m(-2).
The signaling pathways that lysophosphatidic acid (LPA) and sphingosine-1-phosphate (S1P) use to activate Akt in ovarian cancer cells are investigated here. We show for the first time, with the use of both pharmacological and genetic inhibitors, that the kinase activity and S473 phosphorylation of Akt induced by LPA and S1P requires both mitogen-activated protein (MAP) kinase kinase (MEK) and p38 MAP kinase, and MEK is likely to be upstream of p38, in HEY ovarian cancer cells. The requirement for both MEK and p38 is cell type-and stimulusspecific. Among 12 cell lines that we tested, 11 respond to LPA and S1P and all of the responsive cell lines require p38 but only nine of them require MEK. Among different stimuli tested, platelet-derived growth factor stimulates S473 phosphorylation of Akt in a MEK-and p38-dependent manner. However, epidermal growth factor, thrombin, and endothelin-1-stimulated Akt S473 phosphorylation require p38 but not MEK. Insulin, on the other hand, stimulates Akt S473 phosphorylation independent of both MEK and p38 in HEY cells. T308 phosphorylation stimulated by LPA/S1P requires MEK but not p38 activation. MEK and p38 activation were sufficient for Akt S473 but not T308 phosphorylation in HEY cells. In contrast to S1P and PDGF, LPA requires Rho for Akt S473 phosphorylation, and Rho is upstream of phosphatidylinositol 3-kinase (PI3-K). LPA/S1P-induced Akt activation may be involved in cell survival, because LPA and S1P treatment in HEY ovarian cancer cells results in a decrease in paclitaxel-induced caspase-3 activity in a PI3-K/ MEK/p38-dependent manner.
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