新疆哈萨克族儿童超重肥胖与血清超敏C-反应蛋白及胰岛素抵抗指数的相关研究

目的探讨新疆哈萨克族超重、肥胖学龄儿童血清超敏C-反应蛋白(hsCRP)、胰岛素抵抗指数(HOMA-IR)变化及临床意义。方法 2009年5月至2009年7月采用随机分层整群抽样的方法调查新疆伊犁哈萨克族自治州2475名6～14岁哈萨克族在校学生,对其中122例超重或肥胖儿童(超重、肥胖组)及119例年龄、性别相匹配的非肥胖儿童(对照组)分别测体重指数(BMI)、hsCRP、空腹血糖(FPG)、空腹胰岛素(FINS),计算HOMA-IR,比较两组差异及各指标的相关性。结果超重、肥胖组hsCRP、FINS、HMOA-IR明显高于对照组;FPG、低密度脂蛋白(LDL)、总胆固醇(CHO)、高密度脂蛋白(HDL)两组间差异无统计学意义。Pearson相关分析示,BMI与hsCRP、HMOA-IR、FINS有显著正相关趋势,与FPG有负相关趋势,但相关性无统计学意义(P0.05)。与CHO、HDL、LDL有正相关趋势,但相关性无统计学意义(P0.05)。多重线性回归显示,FINS、HMOA-IR、hsCRP、FPG、LDL均与BMI相关。结论新疆哈萨克族超重、肥胖儿童存在胰岛素抵抗,同时炎症因子CRP与新疆哈萨克族儿童超重、肥胖的发生及发展有密切关系。     

瘦素和脂联素在儿童肥胖相关性高血压发病中的作用

目的探讨瘦素和脂联素在儿童肥胖相关性高血压发病中的作用。方法基于北京市儿童青少年代谢综合征研究项目的现况调查结果，非随机选择3 502名6~18岁学龄儿童（其中男1 784名，女1 718名）为研究对象，按照超重（包括肥胖）和高血压状态将研究对象分为4组，正常体重正常血压组（对照组，1 497名）、正常体重高血压组（HBP组，125名）、超重但血压正常组（OB组，1 349名）和超重合并高血压组（OB+HBP组，531名）。通过比较4组人群血清瘦素和脂联素水平，以及瘦素和脂联素与血压之间的相关回归分析，探讨其与肥胖和血压之间的关系。结果超重肥胖人群BMI、血压、胰岛素和瘦素水平显著升高，脂联素水平降低。HBP组与对照组BMI、瘦素、脂联素水平差异无统计学意义。OB组和OB+HBP组与对照组比较，BMI、SBP、DBP、胰岛素和瘦素水平升高，脂联素水平降低，与HBP组比较仍可见BMI、胰岛素和瘦素水平升高，脂联素水平降低。与OB组比较，OB+HBP组BMI和胰岛素水平及男性的瘦素水平明显升高。血压与年龄、BMI、胰岛素、瘦素均呈显著正相关（r=0.260~0.643,P<0.01），与脂联素呈显著负相关（r=-0.171~-0.332, P<0.01）。但在调整胰岛素或BMI后，瘦素、脂联素与血压的相关性减弱或消失。结论 超重人群血压、胰岛素及瘦素水平均高于对照人群，脂联素水平低于对照人群。瘦素、脂联素可能通过肥胖或胰岛素抵抗与血压相关。     

瘦素/脂联素值与肥胖儿童体质量指数及糖脂代谢的关系

目的 探讨瘦素/脂联素(L/A)值与单纯性肥胖儿童体质量指数(BMI)、糖脂代谢及肥胖症发病的关系.方法 单纯性肥胖60例和57例健康儿童,采用放射免疫分析(RIA)法测定其血清瘦素水平;ELISA法测定其血清脂联素、空腹胰岛素(FINS)水平;免疫比浊法测定其血脂各成分.分析并比较血清瘦素、脂联素及L/A值与肥胖儿童BMI、糖脂代谢的相关性.结果 1.肥胖儿童血清瘦素、FINS和三酰甘油(TG)水平与健康对照组相比明显增加;脂联素水平降低,差异均有显著性(Pa＜0.05,0.01).2.单纯性肥胖儿童瘦素与BMI、FINS、TG水平均呈显著正相关(r=0.408,0.301,0.301 Pa＜0.05,＜0.01);脂联素水平与BMI、FINS、TG均呈显著负相关(r=-0.360,-0.413,-0.258 Pa＜0.01,＜0.05).3.L/A值与BMI、FINS、TG呈显著正相关(r=0.780,0.764,0.601 Pa＜0.001).结论 血清瘦素和脂联素与肥胖儿童的发病有关,可作为儿童肥胖的监控指标;L/A值较单独瘦素、脂联素更能反映肥胖症儿童的代谢状况,可为肥胖症儿童糖脂代谢提供更为有效的监测指标.     

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目的观察单纯性肥胖儿童和健康正常体重儿童血清脑源性神经营养因子(BDNF)质量浓度的差异,探讨BDNF与儿童肥胖及瘦素抵抗、胰岛素抵抗的关系。方法南京军区福州总医院儿科等于2004年5月至2005年5月应用酶联免疫法检测单纯性肥胖儿童(37例)和健康儿童(31例)血清BDNF质量浓度与胰岛素(INS)浓度,应用放射免疫法检测血清瘦素(LEP)质量浓度。比较两组儿童血清BDNF、INS、LEP的差异,分析血清BDNF质量浓度与血清LEP质量浓度和INS浓度的关系。结果(1)两组儿童的体重指数(BMI)、BDNF、INS及LEP均差异显著(BMI:F=175·05,P<0·01;BDNF:F=12·35,P<0·01;INS:F=21·71,P<0·01;LEP:F=48·89,P<0·01),肥胖组BMI、INS及LEP均明显高于健康组,而肥胖组BDNF明显低于健康组。(2)影响LEP的因素依次为BMI、丙氨酸转氨酶(ALT)、BDNF(R2=0·5946,F=0·31,P<0·01);影响INS的因素依次为BMI、BDNF(R2=0·2647,F=11·34,P<0·01)。去除BMI、ALT影响后,BDNF与LEP、INS负相关(BDNF与LEP:r=-0·2455,P<0·05;BDNF与INS:r=-0·2878,P<0·05)。结论(1)肥胖儿童血清BDNF缺乏,未发现“BDNF抵抗”的特点。(2)学龄前儿童血清LEP、INS受BMI影响最大,还受血清BDNF影响。BDNF是二者独立的负相关因素。     

单纯性肥胖儿童血清胰岛素水平与瘦素、肿瘤坏死因子-α的关系

目的探讨单纯性肥胖儿童血清胰岛素水平与瘦素（LP）、肿瘤坏死因子-α（TNF-α）的关系。方法肥胖儿童47例依据空腹血清胰岛素和空腹血糖水平,分为高胰岛素血症组（HIG）23例。男16例,女7例;年龄（11.3±2.0）岁。正常胰岛素水平组（NIG）24例。男15例,女9例;年龄（11.8±2.7）岁。并选取同年龄段非肥胖正常儿童10例为健康对照组（NCG）。测量各组身高、体质量、腰围等,检测空腹血清胰岛素（FINS）、LP及TNF-α水平,并计算相关指标,分析它们之间的关系。结果1.HIG组BMI、腰围、臀围、腰臂比（WHR）、LP、TNF-α、胰岛素抵抗指数（HOMA-IR）明显高于NIG组及NCG组（Pa〈0.05,0.01）;胰岛素敏感指数（HOMA-IAI）低于NIG和NCG组（P〈0.05,0.01）;2.与NCG组比较,NIG组BMI、腰围、臀围、WHR、LP、HOMA-IR明显增高（Pa〈0.05,0.01）,HOMA-IAI显著降低（P〈0.05）,TNF-α、空腹血糖（FBG）比较差异不显著（Pa〉0.05）;3.HIG组FINS与LP、TNF-α、HOMA-IR分别呈显著正相关（r=0.560,0.413,0.846 P〈0.01,0.05,0.01）,与HOMA-IAI呈显著负相关（r=-0.823P〈0.01）,与血糖无相关性。LP、TNF-α与IR独立相关。结论肥胖患儿血清胰岛素水平与LP、TNF-α密切相关,LP、TNF-α致胰岛素抵抗可能是肥胖患儿高胰岛素血症的原因之一。     

伴阻塞性睡眠呼吸暂停低通气综合征的肥胖儿童血清瘦素和脂联素水平变化的意义

目的探讨伴阻塞性睡眠呼吸暂停低通气综合征(OSAHS)肥胖儿童血清瘦素(LP)和脂联素(AP)水平及其相关性。方法选择经多导睡眠记录仪(PSG)确诊的41例OSAHS患儿,将其分为OSAHS肥胖组(21例)、OSAHS非肥胖组(20例);另选保健科门诊就诊的28例儿童分为单纯肥胖组(18例)和健康对照组(10例)。采用放射免疫法检测各组儿童血清LP和AP水平,并分析OSAHS肥胖患儿血清LP和AP水平与体质量指数(BMI)、呼吸睡眠紊乱指数(AHI)的相关性。结果单纯肥胖组、OSAHS非肥胖组、OSAHS肥胖组血清LP水平依次升高,且均高于健康对照组(Pa<0.05),血清AP水平则依次减低,且均显著低于健康对照组(Pa<0.05);OSAHS肥胖组血清LP水平分别与BMI、AHI呈显著正相关(r=0.59,0.79 Pa<0.01),血清AP水平与BMI、AHI及LP水平呈显著负相关(r=-0.59,-0.67,-0.76 Pa<0.01)。结论OSAHS肥胖患儿血清LP水平升高、AP水平减低与其体内存在LP抵抗和AP合成反馈调节机制障碍有关,LP、AP、肥胖与儿童OSAHS有独立的相关性。     

单纯性肥胖症儿童糖耐量及胰岛素分泌功能测定

目的　了解单纯性肥胖症儿童胰岛素分泌功能与糖耐量减低 (IGT)的发生。方法　测定单纯性肥胖症儿童 3 0例空腹及餐后血糖、胰岛素水平。如空腹血糖 (FPG) <6.1mmol/L ,服糖后 2h血糖≥ 7.8mmol/L并 <11mmol/L即为IGT ,若服糖后 2h血糖 <7.8mmol/L为糖耐量正常 (NGT)。计算胰岛素敏感性指数。结果　葡萄糖耐量 (OGTT)结果显示 ,单纯性肥胖症例 3 0中 ,IGT 14例 ( 48% ) ;肥胖儿童FPG( 4.92±1.2 3mmol/L)和正常儿童 ( 4.5 1± 0 .5 8mmol/L)无差异 (P >0 .0 5 ) ;空腹胰岛素 (FINS) ( 3 0 .99± 2 7.71) μIU/L水平明显高于正常儿童 ( 10 .2 3± 2 .3 5 ) (P <0 .0 1)。胰岛素敏感性指数 (IAI) ( - 5 .0 2± 0 .2 3 )明显低于正常儿童 ( - 3 .83± 0 .19) (P <0 .0 1)。肥胖儿童IGT组BMI、FINS、FPG较NGT组高 ,无显著性差异 (P >0 .0 5 ) ;服糖 2h胰岛素 (INS 2 )及 2h血糖明显高于NGT组 (P <0 .0 1) ;IGT组ISI(由OGTT计算 )明显低于NGT组 (P<0 .0 0 1)。 3 0例肥胖儿童BMI与FINS、INS2、2h血糖明显正相关 (分别为r =0 .69　P <0 .0 1;r =0 .41　P <0 .0 5 ;r =0 .3 9　P <0 .0 5 ) ,与ISI明显负相关 (r =- 0 .3 8　P <0 .0 5 )。结论　肥胖儿童存在明显的胰岛素抵抗现象 ,且肥胖程度越重 ,机体对胰岛素     

肥胖儿童运动减肥治疗前后的瘦素抵抗血脂及炎症状态分析

目的：研究显示C-反应蛋白（CRP）、瘦素(Lp)、可溶性瘦素受体(sLR) 及多种血脂成分均参与了肥胖的发生发展。本研究旨在探讨运动减肥治疗前后肥胖儿童瘦素抵抗、血脂及炎症状态的改变,以期明确运动对肥胖儿童内分泌环境的影响。方法：对51例12岁肥胖儿童进行为期2月的运动减肥治疗,观察血清高敏C反应蛋白（hs-CRP）、Lp、sLR、甘油三酯(TG)、总胆固醇(TC)及低密度脂蛋白胆固醇(LDL-C)水平变化。40例健康体检儿童作为对照组。结果：肥胖儿童组血清Lp、TG、TC、LDL-C和hs-CRP水平及体重指数（BMI）均显著高于对照组（均P<0.01）,sLR水平低于对照组（P<0.05）。运动减肥治疗后肥胖儿童组血清hs-CRP、Lp、TC、TG和LDL-C水平及BMI与治疗前比较显著下降（P<0.05）。相关性分析显示肥胖儿童血清Lp水平与血脂及hs-CRP呈显著正相关（P<0.05）;Lp、hs-CRP与sLR呈显著负相关（P<0.05）;hs-CRP与血脂呈显著正相关（P<0.01）。结论：肥胖儿童已存在瘦素抵抗及血脂和炎症状态的改变,运动减肥治疗可不同程度地改善这些改变。［中国当代儿科杂志,2010,12（1）：40-42］     

儿童肥胖与代谢综合征的相关性

目的 探讨儿童肥胖与代谢综合征(MS)各指标的关系.方法 选择60例肥胖患儿作为肥胖组,60例正常体质量儿童作为健康对照组,比较2组体质量指数(BMI)、腰围与身高比(WHtR)、平均动脉压(MAP)、三酰甘油(TG)、空腹胰岛素(FIS)、血尿酸(UA)、脂蛋白(LP)及胰岛素敏感指数(ISI)和抵抗指数(IRI)等MS指标,并进行统计学处理.结果 肥胖组BMI、WHtR、MAP、TG、FIS、UA、LP及ISI、IRI均显著高于健康对照组,差异均有统计学意义(Pa<0.05).结论 肥胖儿童存在胰岛素抵抗及脂血谢紊乱,并有血压、血UA升高.对处于生长发育期的儿童,应控制和预防肥胖发展,以降低MS及成年时糖尿病、冠心病的发生.     

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目的探讨血清脂联素水平与高胰岛素血症和(或)胰岛素抵抗的联系。方法采用酶联免疫法测定2004-02—2004-12在天津医科大学总院就诊的34例肥胖儿童和31例正常对照的血清脂联素水平。分析血清脂联素与人体参数、体脂分布及糖代谢中各指标的相关关系。结果(1)肥胖组脂联素水平低于对照组(P<0.001)。(2)脂联素与性别、年龄无相关关系;与收缩压、舒张压呈负相关(相关系数分别为r=-0.369,r=-0.405,P<0.01);与BMI、腰臀比和SF呈负相关(相关系数分别为r=-0.330,r=-0.282和r=-0.350,P<0.01);与空腹血糖、空腹胰岛素水平呈负相关(相关系数r=-0.264和r=-0.357,P<0.01);与HOMA-R呈负相关(P<0.01),与HOMA-β无相关关系。(3)多元回归分析表明,HOMA-R是影响脂联素最为显著的因素,R2=0.122;标准化偏回归系数-0.369(P<0.01)。结论肥胖症儿童血清脂联素水平较正常儿童降低。血清脂联素水平的变化,是影响空腹血糖、空腹胰岛素水平、HOMA-R的重要因素。低脂联素血症可能参与胰岛素抵抗的发生。     

Are C‐reactive protein and homocysteine cardiovascular risk factors in obese children and adolescents?

Background: Several prospective epidemiological studies have demonstrated that high-sensitivity C-reactive protein (hsCRP) and plasma homocysteine (hcy) are predictors of future coronary events among healthy men and women. The aim of the present study was therefore to investigate a possible relationship between hsCRP, hcy levels and body mass index (BMI), relative weight (RW), serum leptin levels, and cardiovascular risk factors in obese children and adolescents.
Methods: The study involved 28 obese children and adolescents (13 girls, 15 boys; BMI>95‰ for age and sex), 4.5–15 years of age (mean 10.7 ± 0.6 years), who attended hospital for a basic obesity check-up. The association between hsCRP, hcy levels and BMI, RW, serum leptin levels, and cardiovascular risk factors such as blood pressure (BP), lipid profile, serum fasting insulin levels, and insulin resistance indexes, was investigated.
Results: Serum hsCRP level was positively correlated with BMI ( r = 0.512, P  < 0.01), RW ( r = 0.438, P  < 0.05), systolic and diastolic BP ( r = 0.498, P  < 0.01), serum leptin levels ( r = 0.457, P  < 0.05), but not with serum lipid, glucose, fasting insulin, plasma hcy levels or insulin resistance indexes. For hcy level, in contrast, no correlation was found with BMI, RW, systolic and diastolic BP, serum lipid levels, leptin, hsCRP, glucose, fasting insulin levels, or insulin resistance indexes.
Conclusions: hsCRP is correlated with BMI, RW, BP and leptin, which are risk factors for coronary heart disease, which supports the relationship between obesity, inflammation and atherosclerosis. hsCRP in childhood obesity might be a useful index to predict possible atherosclerotic events.     

超敏C-反应蛋白和胰岛素敏感指数在儿童阻塞性睡眠呼吸暂停综合征中的变化

目的：探讨阻塞性睡眠呼吸暂停综合征（OSAHS）患儿超敏C-反应蛋白（hsCRP）和胰岛素敏感指数（ISI）的变化。方法：51例患儿分为 OSAHS组（29例）和原发性鼾症（PS）组（22例）。均实施多导睡眠监测仪（PSG）检测,分别测体重指数（BMI）、hsCRP、血脂、空腹血糖(FPG)、空腹胰岛素(INS),计算ISI。结果：与 PS 组比较,OSAHS组的呼吸暂停通气指数（AHI）增高（13.2±9.2 vs 1.2±1.1, P<0.05）;OSAHS组的最低血氧饱和度（LSaO2）低于PS患儿［(78.5±5.4)% vs (87.4±3.7)%, P<0.05］;OSAHS组的hsCRP高于PS组（2.8±2.7 mg/L vs 0.6±0.9 mg/L,P<0.05）;OSAHS组的ISI、血脂与 PS 组的差异无统计学意义。OSAHS 组的hsCRP与LSaO2呈负相关（r=-0.531, P<0.05）。结论：OSAHS患儿hsCRP水平增高,可能与日后心血管疾病的发生相关,应早期给予干预。     

肥胖儿童瘦素水平的变化及其与骨密度的关系

目的：探讨长沙市肥胖儿童血清瘦素水平的变化及与骨密度（BMD）、身体成分的关系,为预防和治疗儿童肥胖及骨质疏松提供科学依据。方法：从长沙市5所小学随机抽取119例肥胖儿童和103例正常儿童,采用双能X线骨密度仪（DEXA）进行全身扫描,测定骨密度及身体成分;采用酶联免疫吸附试验（ELISA）测定血清瘦素水平。结果：①肥胖儿童的身高、体重、体重指数（BMI）、腰围和腰臀比均显著高于正常儿童（P<0.01）。②肥胖儿童的全身骨密度、骨矿物质含量、瘦组织含量、脂肪组织含量、体脂百分比(%BF)及血清瘦素水平均显著高于正常儿童（P<0.01）。③血清瘦素水平与儿童全身骨密度、骨矿物质含量、瘦组织含量、脂肪组织含量均呈显著正相关（r=0.528~0.903）,其中瘦素水平与脂肪组织含量呈高度正相关（男：r=0.883,女：r=0.903）。多元逐步回归分析显示,BMI及%BF是儿童血清瘦素水平的独立影响因素。结论：肥胖儿童血清瘦素水平升高,血清瘦素水平与骨密度及身体成分显著相关,BMI、%BF是儿童血清瘦素水平的独立影响因素。［中国当代儿科杂志,2009,11（9）：745-748］     

Leptin binding activity (LBA) in plasma of nondiabetic and diabetic adolescents and obese children: relation to auxologic and hormonal data

Leptin circulates in serum bound to high molecular weight proteins. Hypothesizing that leptin binding proteins may regulate the functional efficiency of leptin, we characterized auxologic and hormonal factors that influence leptin binding in three disparate groups: normal adolescents, obese children, and teenagers with type I diabetes mellitus (IDDM). Specific leptin binding activity (sLBA) was assessed by column chromatography after incubation of serum with 125I-leptin in the presence and absence of excess unlabeled leptin. Mean sLBA was 17.0 +/- 7% (SD) in the healthy adolescents (n=41), 6.6 +/-4.3% in the obese children (n=26), and 14.9 +/-7.3% in the diabetic teenagers (n=17). At any value of sLBA, obese children had higher serum leptin levels than non-obese adolescents or diabetic teenagers, consistent with "leptin resistance" in the obese group. sLBA was higher in males than in females only in those with diabetes (18.6 +/- 7.3 vs 10.9 +/- 5.1%, p<0.05). sLBA correlated inversely with serum insulin-like growth factor-I values in the normal group (r= -0.45, p<0.01) and with insulin in the obese children (r= -0.53, p<0.01). There was no correlation between sLBA or serum leptin values and HbA1c, in the diabetic group. The serum leptin concentration was the principal determinant explaining the total variability of sLBA in all three cohorts. However, body mass index (BMI = weight/ height2) accounted for more of the total variability of percent specific binding in the healthy adolescents than in the other groups. We conclude that sLBA reflects circulating leptin levels, body composition, and hormonal milieu. Thus, in addition to leptin, qualitative and quantitative characteristics of leptin binding may play a physiological role in the regulation of appetite and in the "leptin resistance" of obesity.     

Correlates of adiponectin and the leptin/adiponectin ratio in obese and non-obese children

Adiponectin is an adipocyte secreted protein that has been reported to increase fatty acid oxidation and improve insulin sensitivity. Our aim was to study the relationship between adiponectin and leptin, body fat, insulin and lipoproteins in obese compared to non-obese children matched for age and gender. Adiponectin serum concentrations were significantly lower in the obese compared to the non-obese children (9.1+/-3.7 vs 17.1+/-12.3 microg/ml, p <0.05), in contrast to serum leptin concentrations which were greater in the obese compared to the non-obese subjects (31.8+/-11.1 vs 8.2+/-5.7 ng/ml, p <0.001). When considered as a single group to assess adiponectin concentrations over a spectrum of body size, adiponectin values correlated inversely with body weight (r = -0.33, p <0.05) and BMI (r = -0.35, p <0.05). Adiponectin values correlated directly with HDL-C (r = 0.47, p <0.005), but not with total cholesterol, IGF-I, or leptin binding activity. Since leptin and adiponectin change inversely in relation to BMI, the leptin/adiponectin (L/A) ratio was determined as a potential index relating adiposity to the development of complications of obesity. The L/A ratio was eight-fold greater in the obese compared to the non-obese children, and correlated more strongly with BMI (r = 0.779, p <0.0001) and with HDL-C (r = -0.53, p <0.001), than did adiponectin alone. The L/A ratio also correlated significantly with triceps skinfold thickness (TSF) (r = 0.77, p <0.001) and percent body fat (r = 0.79, p <0.0001) in non-obese children. These data suggest that adiponectin concentrations are already differentially regulated in childhood obesity. The index of increased leptin concentration corrected by reduced adiponectin values (L/A ratio) merits investigation as a marker for morbidities associated with childhood obesity.     

Changes in leptin, insulin and body composition in obese children during a weight reduction program

BACKGROUND: Girls have higher leptin concentrations than boys at all stages of biological development and this is also seen in the state of obesity. Little is known about whether gender and biological development of obese children influence changes in leptin associated with a short-term weight reduction program. OBJECTIVE: To study whether leptin concentration, body composition and insulin levels in obese children were influenced by a 3-week intervention program including diet and sports. STUDY DESIGN: Sixty-two obese children (32 boys and 30 girls) were examined before and after the intervention program. Body composition was measured by bioelectrical impedance and BMI-SDS was calculated. Serum leptin and serum insulin were determined by RIA. RESULTS: Girls had higher leptin levels than boys, before and after the weight reduction program. Body mass, fat mass (FM), leptin and insulin were decreased after the intervention in both sexes. We found a greater change in serum leptin in girls but the change in FM was of greater magnitude in boys. However, percentage changes in leptin were not significantly different between the sexes. Before the intervention, leptin concentrations were correlated with %FM, FM and moderately with BMI-SDS in all children. Only in pubertal boys did correlation of leptin with %FM increase after the intervention (from r=0.57 to r=0.75, p<0.01). Changes in leptin were found to be associated with initial leptin values in boys (r=0.95, p<0.01) and in girls (r=0.93, p<0.01), independent of Tanner stages. CONCLUSION: Serum leptin levels were positively correlated with adiposity in obese children and a diet and sports intervention program decreased serum leptin, insulin and body fat in all children. Changes in leptin were best described by the initial leptin concentration. The increase in correlation of leptin with %FM in obese pubertal boys after the intervention could have its underlying mechanism in an increased sensitivity to leptin and anabolic hormones.     

肥胖幼鼠脂肪组织vaspin与胰岛素敏感性的关系

目的：探讨幼年肥胖Sprague-Dawlely（SD）大鼠脂肪组织vaspin含量与胰岛素敏感性的关系。方法：断乳3周SD大鼠24只,随机分为高脂饮食组和普通饮食组,每组12只。成功建模后,测定各组体重、腹围。禁食12 h 后取内眦静脉血测定空腹血糖（FPG）、空腹胰岛素（FINS）;再腹腔注射50%葡萄糖（2 g/kg）,于注射后60 min、120 min再次取内眦静脉血测定各时间点血糖（BG）及胰岛素（INS）。幼鼠处死后将内脏脂肪组织称重。酶联免疫吸附法测定各组幼鼠内脏脂肪组织中vaspin的含量,并对vaspin表达量与各体格测量指标及胰岛素敏感性评价指标进行相关性分析。结果：高脂饮食组大鼠的体重、腹围、内脏脂肪重量、FPG、FINS、120 min INS、vaspin、胰岛素抵抗指数（HOMA-IR）、胰岛素分泌指数（HOMA-β）均高于普通饮食组（P<0.05）,高脂饮食组胰岛素敏感指数（ISI）明显低于普通饮食组（P<0.01）。Vaspin含量与肝脏重量、内脏脂肪重量、腹围、120 min INS、FPG、FINS、HOMA-IR、HOMA-β呈正相关（P<0.05）,而与ISI呈负相关（P<0.05）。结论：幼年肥胖SD大鼠胰岛素抵抗状态与vaspin高水平表达有关,推测vaspin是一种增加胰岛素敏感性、促进胰岛β细胞分泌胰岛素和改善糖耐量的脂肪细胞因子,可能参与了胰岛素抵抗、糖代谢紊乱状态的形成。     

不同指标在评价肥胖儿童胰岛素抵抗中的价值

目的探讨单纯性肥胖儿童胰岛素抵抗临床评估的指标。方法对单纯性肥胖和正常对照儿童进行葡萄糖耐量试验和胰岛素释放试验,在试验前及试验后30、60、120、180 min分别测血糖和胰岛素,并计算稳态模型胰岛素抵抗指数(HOMA-IR)、敏感指数(HOMA-IAI)、胰岛素分泌功能(HOMA-IS)、血糖曲线下面积与胰岛素曲线下面积比及空腹血糖和空腹胰岛紊的比值(FBG/FINS)等胰岛素抵抗评价指标。结果肥胖组FINS明显高于对照组,FBG、HOMA-IS与对照组无显著差异。HOMA-IR和HOMA-IAI之间具有显著相关性,r为-1,与FINS的r分别为0.913和-0.913,与FBG/FINS的r分别为-0.889和0.889,与曲线下面积比的r分别为-0.523和-0.523,P均<0.01。结论FINS、HOMA-IR、HOMA-IAI、血糖与胰岛素曲线下面积比、FBG/FINS均适用于肥胖儿童胰岛素抵抗的评估,尤以FINS、HOMA-IR、HOMA-IAI更可取。