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目的探寻肥胖与糖脂代谢异常的相关性及相应靶器官肝脏、心脏损害情况,以早期采取干预措施。方法选择2008年7月至2010年10月沈阳市儿童医院儿保门诊就诊的单纯性肥胖儿童516例为肥胖组,100名体检体重正常儿童为对照组。取空腹静脉血检测空腹血糖(FPG)、甘油三酯(TG)、总胆固醇(TC)、谷丙转氨酶(ALT)、空腹胰岛素(FINS)等指标,计算胰岛素抵抗指数(HOMA-IR)及胰岛β细胞功能值(HOMA-β);对肥胖儿童行口服糖耐量试验(OGTT)和胰岛素释放试验。对所有入组者均进行肝脏和心脏超声检查。结果肥胖组收缩压、舒张压均高于对照组(P<0.05),肥胖组高血压检出率为12.0%(62/516)。肥胖组FBG、FINS、HOMA-IR及HOMA-β均高于对照组(P<0.05);TC、TG、LDL-C均高于对照组,而HDL-C低于对照组,差异均有统计学意义(P<0.05)。轻、中、重度肥胖组脂肪肝发生率差异有统计学意义(P<0.001),且随肥胖程度加重,脂肪肝发生率明显增加(χ2=12.97,P<0.001)。肥胖组心包外脂肪增厚268例,平均厚度(3.372±0.098)mm,与对照组比较差异有统计学意义(P<0.001)。97例代谢综合征(MS)患儿进行饮食控制、加强运动,结合口服二甲双胍药物等早期联合干预治疗,FINS和HDL-C改善差异有统计学意义(P<0.001)。结论肥胖儿童高血压发生风险、糖代谢异常均高于非肥胖儿童,轻度肥胖即可发生FPG受损、糖耐量减低、胰岛素抵抗、高胰岛素血症和β细胞功能减低等糖代谢异常。肥胖儿童有明显的血脂代谢紊乱,易并发脂肪肝,脂肪肝发生率与肥胖严重程度相关,10岁后肥胖儿童脂肪肝发生比例明显升高。肥胖儿童左心室肥大和心包外脂肪增厚明显高于正常体重儿童。联合干预治疗肥胖儿童可明显降低FINS和升高HDL-C值,可防止其发展为糖耐量减低和糖尿病。
Objective To explore the correlation between obesity and abnormal glucose and lipid metabolism and the damage of liver and heart of the corresponding target organ, and to take early intervention. Methods A total of 516 simple obesity children admitted to Children’s Hospital of Shenyang Children’s Hospital from July 2008 to October 2010 were selected as obese group and 100 normal weight-bearing children as control group. The fasting blood glucose (FPG), triglyceride (TG), total cholesterol (TC), alanine aminotransferase (ALT) and fasting insulin (FINS) were measured in fasting venous blood to calculate the index of insulin resistance (HOMA-IR) and islet β cell function value (HOMA-β); oral glucose tolerance test (OGTT) and insulin release test in obese children. All subjects underwent liver and cardiac ultrasound. Results The systolic blood pressure and diastolic blood pressure in obese group were higher than those in control group (P <0.05). The prevalence of hypertension in obese group was 12.0% (62/516). The levels of FBG, FINS, HOMA-IR and HOMA-β in obesity group were significantly higher than those in control group (P <0.05). The levels of TC, TG and LDL-C in obesity group were higher than those in control group Significance (P <0.05). There was significant difference in the incidence of fatty liver in mild, moderate and severe obesity group (P <0.001), and with the increase of obesity, the incidence of fatty liver increased significantly (χ2 = 12.97, P <0.001). There were 268 cases of pericardial fat thickening in obese group with an average thickness of (3.372 ± 0.098) mm, which was significantly different from the control group (P <0.001). 97 cases of metabolic syndrome (MS) children diet control, exercise, combined with oral metformin and other early joint intervention, FINS and HDL-C improvement difference was statistically significant (P <0.001). Conclusions Obese children have higher risk of developing hypertension and abnormal glucose metabolism than non-obese children. Mild obesity can cause abnormal glucose metabolism such as impaired glucose tolerance, impaired glucose tolerance, insulin resistance, hyperinsulinemia and β-cell function. Obese children have obvious dyslipidemia, easy to complicated with fatty liver, the incidence of fatty liver and the severity of obesity, obese children after 10 years of age, the incidence of fatty liver increased significantly. Obese children with left ventricular hypertrophy and pericardial fat thickening was significantly higher than normal weight children. Combined treatment of obese children can significantly reduce the FINS and increase HDL-C values, to prevent the development of impaired glucose tolerance and diabetes.