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First, obesity, metabolic syndrome pups modeling and liver tissue 5α-reductase 1 and 11β-hydroxysteroid dehydrogenase 1 Objective: In the first part of this study, the high-fat, high-fat, high-salt diet induced insulin resistance, lipid metabolism disorders. Observation of different diets on body fat distribution, insulin sensitivity and metabolic indicators of impact, in order to build the metabolic syndrome in young rats model. Explore the metabolic syndrome the pups liver the cortisol metabolism key enzyme 5α-reductase and 11β-hydroxysteroid dehydrogenase 1 expression and function of cortisol metabolism. Methods: 50 grams male, female SD rats were randomly divided into three groups: normal diet group (NC group): high-fat group (FC group); fat ten high-salt group (FSC group). Measurement of body weight, body length, abdominal circumference, blood pressure, observation visceral fat weight, blood lipids, blood cortisol, the line oral glucose tolerance test and insulin release test evaluation of blood glucose and islet cell function. Fresh liver tissue, Determination of 5α-reductase and 11β-hydroxysteroid dehydrogenase 1mRNA content and the ratio of the two enzyme mRNA content. Results: high-fat high-salt diet the rat abdominal circumference, blood pressure, visceral fat, fasting glucose, insulin levels than the control group increased significantly, increased dyslipidemia and insulin resistance demonstrated significant. High-fat and high-fat high-salt diet rats 5α-reductase 1 mRNA increased 11β-hydroxysteroid dehydrogenase 1 mRNA decreased, a significant increase in the ratio of the two enzyme mRNA content, these indicators were significantly correlated with blood levels of cortisol. Conclusion: We successfully to high-fat high-salt diet-induced obesity metabolic syndrome in young rats model in rats in vivo insulin resistance and lipid metabolism, waist circumference, blood pressure, body weight, visceral fat weight and metabolic syndrome increased significantly in the underlying index . High expression of liver tissue 5α-reductase 1 and low expression of 11β-hydroxysteroid dehydrogenase 1 can aggravate insulin resistance and dyslipidemia, abnormal glucocorticoid metabolism and regulation related metabolic syndrome may occur. Tip targeted regulation of 5α-reductase 1 and 11β-hydroxysteroid dehydrogenase 1 expression and activity may be a cause of treatment of metabolic syndrome. Obesity metabolic syndrome child cortisol metabolism Objective: To study serum cortisol (COR) in children metabolic syndrome (MS), the significance of the development process, to find where the law. Methods: 96 confirmed in obese children, according to Cook raised the standard of MS, according to waist circumference (WC), blood pressure (BP), blood lipids and glucose were divided into MS group and the non-MS group to collect basic clinical information, measurement anthropometric parameters, serum COR, lipids, underwent oral glucose tolerance test (OGTT) and insulin release test, insulin resistance index (HOMA-IR), and the above information is used for statistical analysis. Results: The serum the COR level of MS group than the non-MS group (P <0.05); correlation analysis prompted COR level WC, systolic blood pressure (SBP), diastolic blood pressure (DBP) and the MS group scores (nMSc) was positively correlated (P <0.05 ), and plasma high density lipoprotein cholesterol (HDL-C) levels were negatively correlated (P <0.05); WC, SBP, DBP regression analysis showed that the significant factors affecting serum COR. Conclusion: The serum COR with insulin resistance and other multi-factors may be involved in MS pathogenesis and progression.
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