0～14岁儿童血肥胖抑素含量及其意义

目的了解0～14岁儿童血肥胖抑素(Leptin) 水平.方法对154名(男 78名,女 76名)0～14岁健康非肥胖儿童(38例)和超重/肥胖儿童(39例)的Leptin分布、性别/年龄变化趋势、与人体测量学参数(腰围、腰臀比、瘦体重、全身体脂含量、体脂百分数、BMI/Kaup指数)和血胰岛素水平的相互关系进行了研究.结果 (1)健康非肥胖儿童Leptin值为1.01～29.92 (ng/ml),均值为2.99±2.13 (ng/ml).90%可信限范围,男童为1.36～14.21 (ng/ml),女童为1.74～21.17 (ng/ml).血浆与血清Leptin值差异无显著意义;(2)超重/肥胖儿童血Leptin值明显高于非肥胖儿童(P＜0.001).(3)Leptin性别差异有显著意义(P=0.023),在非肥胖儿童中更明显(P=0.004).多元回归分析表明,加入体脂因素后性别因素不再与Leptin 水平相关(P=0.138,0.241,0.990),而BMI、体脂含量和体脂百分数的影响差异有显著意义(P＜0.001);(4)Leptin值与年龄存在相关关系(P=0.005),超重/肥胖组更著,女性随年龄增长而升高的趋势更明显(P=0.001).青春期前期Leptin值开始上升,女性明显高于男性(P=0.045).不同年龄组其Leptin值明显不同(P＜0.001).(5)Leptin值与BMI、体脂含量和体脂百分数显著正相关、与瘦体重相关关系弱,男童与腰臀比不相关,女童存在相关关系.曲线回归方程(Quadatic)比直线相关方程更好的指示上述相关.(6)0～7岁儿童Leptin值与出生体重明显相关(P=0.001),自学龄期后无相关关系(P=0.456).(7)Leptin值与空腹胰岛素水平呈正相关(P＜0.001).结论儿童血Leptin值的发育与脂肪发育及重聚规律一致.     

肥胖儿童血浆血管假性血友病因子与动脉粥样硬化指数的相关性分析

目的探讨单纯性肥胖儿童血管内皮凝血功能改变及其与动脉粥样硬化指数(AI)的关系。 方法2004 07 11由山东大学省立医院对济南市区部分小学生查体,从中筛选单纯性肥胖儿童及正常对照儿童各30例。专人测定血压及肥胖相关体格测量指标,测定血脂及血浆血管假血友病因子(vWF),计算体重指数(BMI)、腰臀比(WHR)、动脉粥样硬化指数(AI)。 结果肥胖儿童皮褶厚度、WHR、BMI、收缩压(SBP)、舒张压(DBP)、总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白(LDL)、载脂蛋白B(ApoB)、AI、vWF显著升高,而高密度脂蛋白(HDL)、载脂蛋白A1(ApoA1)则显著下降。vWF与SBP、WHR、TC、AI呈正相关,与ApoA1呈负相关。 结论单纯性肥胖儿童存在血管内皮凝血功能障碍,其与脂代谢紊乱密切相关,增加了发生动脉粥样硬化(AS)及高血压的危险性。     

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目的探讨单纯性肥胖儿童血管内皮凝血功能改变及其与动脉粥样硬化指数(AI)的关系。方法2004-07-11由山东大学省立医院对济南市区部分小学生查体,从中筛选单纯性肥胖儿童及正常对照儿童各30例。专人测定血压及肥胖相关体格测量指标,测定血脂及血浆血管假血友病因子(vWF),计算体重指数(BMI)、腰臀比(WHR)、动脉粥样硬化指数(AI)。结果肥胖儿童皮褶厚度、WHR、BMI、收缩压(SBP)、舒张压(DBP)、总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白(LDL)、载脂蛋白B(ApoB)、AI、vWF显著升高,而高密度脂蛋白(HDL)、载脂蛋白A1(ApoA1)则显著下降。vWF与SBP、WHR、TC、AI呈正相关,与ApoA1呈负相关。结论单纯性肥胖儿童存在血管内皮凝血功能障碍,其与脂代谢紊乱密切相关,增加了发生动脉粥样硬化(AS)及高血压的危险性。     

52例肥胖和超重儿童糖耐量及胰岛素释放试验分析

目的 了解肥胖和超重儿童糖代谢及胰岛细胞功能状况。方法 对52例单纯性肥胖与超重儿童进行口服糖耐量试验,并测定其血糖及胰岛素水平。计算胰岛素抵抗指数(IR),胰岛素敏感指数(IS),服糖后30min胰岛素增加值与血糖增加值的比值。并查甘油三酯、肝脏B超。体重指数(BMI)与IR之间、不同BMI组之间、糖耐量减低组与对照组之间进行比较。结果 发现糖尿病1例(1．9％),IGT者5例(9．6％)。IR≥2．8为胰岛素抵抗,占76．9％。BMI与IR之间无相关关系。不同BMI组之间IR、IS、服糖后30min胰岛素增加值与血糖增加值的比值差异均无统计学意义。糖耐量减低组与对照组之间IR、IS差异无统计学意义,服糖后30min胰岛素增加值与血糖增加值的比值之间差异有统计学意义。甘油三酯升高19例(37％),脂肪肝16例(53％)。结论 肥胖与超重儿童普遍存在胰岛素抵抗和敏感性下降,其与BMI程度无关。肥胖伴糖耐量减低儿童除胰岛素抵抗外存在明显的B细胞功能减退。许多肥胖和超重儿童同时存在脂代谢紊乱。     

瘦素及可溶性瘦素受体在原发性肾病综合征患儿血脂升高中的作用

目的探讨瘦素(Leptin)及可溶性瘦素受体(sOBR)在儿童原发性肾病综合征(PNS)血脂升高中的作用。方法检测23例未经治疗的PNS患儿空腹血清血脂、血浆清蛋白、Leptin、sOBR、胰岛素及尿Leptin、sOBR水平,并与在年龄、性别、体质量指数(BMI)均匹配的15例正常儿童比较。结果肾病组血胆固醇(TC)、三酰甘油(TG)、低密度脂蛋白(LDL)、载脂蛋白B(apoB)水平增高,血浆清蛋白、胰岛素水平较对照组降低。空腹血清总Leptin水平肾病组与对照组相当,而尿Leptin水平肾病组高于对照组;血清sOBR水平肾病组降低,尿sOBR水平二者无差异;血清游离Leptin指数(FLI)肾病组高于对照组。肾病组游离Leptin指数(FLI)与血浆清蛋白、HDL、apoA呈正相关,与LDL、胰岛素呈负相关。结论PNS患儿血清sOBR减少,游离瘦素增多可能为一抗高脂血症的代偿机制,但其纠正PNS脂代谢紊乱的能力并不完全。     

血清谷丙转氨酶与儿童超重、肥胖的关系

目的：探讨血清谷丙转氨酶（ALT）与儿童超重、肥胖的关系。方法：对年龄7～18岁的2889例正常儿童及702例超重、肥胖儿童的资料进行分析,测量身高、体重、腰围、血压,检测空腹血糖、血脂、ALT、胰岛素等生化指标,计算胰岛素抵抗指数。结果：男童ALT水平高于女童。随着体重指数（BMI）的增加,男女童正常组、超重组、肥胖组ALT水平均逐渐增加。ALT与BMI、腰围、甘油三酯、胰岛素抵抗指数等相关。在超重、肥胖儿童中,男童ALT升高组BMI、腰围、血压、甘油三酯、低密度脂蛋白、胰岛素抵抗指数均较ALT正常组高（P<0.05）;女童ALT升高组腰围、血压、胰岛素抵抗指数高于ALT正常组,而高密度脂蛋白降低（P<0.05）。结论：ALT与儿童超重、肥胖及其引起代谢异常如血脂异常、胰岛素抵抗相关。     

肥胖症儿童血清抵抗素水平与胰岛素抵抗关系的研究

目的探讨肥胖症儿童血清抵抗素水平与高胰岛素血症和(或)胰岛素抵抗的关系。方法采用酶联免疫法测定34例肥胖儿童,31例正常对照的血清抵抗素水平。分析血清抵抗素与体重指数、体脂百分比、腰臀比及空腹血糖、空腹胰岛素水平、胰岛素抵抗指数、胰岛β细胞功能指数的相关关系。结果(1)肥胖组及对照组抵抗素浓度(对数转换值3.1±0.5)高于对照组(对数转换值2.7±0.8)(P<0.05)。(2)抵抗素与性别、年龄、收缩压、舒张压无相关关系;与体重指数、体脂百分比、腰臀比呈正相关(相关系数分别为r=0.299、0.304、0.322,P<0.01);与空腹血糖及空腹胰岛素水平呈正相关(相关系数为r=0.299和r=0.303,P<0.05);与胰岛素抵抗指数呈正相关(r=0.324,P<0.01),与胰岛β细胞功能指数无相关关系。(3)多元逐步回归分析表明,胰岛素抵抗指数为影响抵抗素最为显著的因素(R2=0.105);标准化偏回归系数0.279(P<0.01)。结论肥胖症儿童血清抵抗素水平较正常儿童增高,并与肥胖程度,脂肪分布密切相关。抵抗素可能与肥胖症儿童发生高胰岛素血症和(或)胰岛素抵抗有关。     

应用传统超声和多普勒组织显像检测单纯性肥胖小儿左心结构和左心功能

目的 明确儿童期单纯性肥胖对心血管系统的影响。方法 应用传统超声和彩色多普勒组织显像技术(DTI)全面检测63例7-14岁中重度单纯性肥胖儿童及63例正常体重对照儿童的左心解剖和功能,并分析其与肥胖程度的关系。结果 ①肥胖组左室舒张内径、室间隔和左室后壁厚度、左室心肌重量(LVM)显著增加(P<0.01),而LVM指数(LVMI,LVM／体表面积)无明显变化(P＞0.05);搏血指数和心脏指数显著降低(P＜0.01＝;二尖瓣环血流速度A峰,E／A,左室后壁舒张早期内外膜运动速度差值(DME),二尖瓣环舒张早期运动速度(DeV),舒张晚期运动速度(DaV),舒张早晚期运动速度比(DeV／aV)均有显著改变(P<0.01)。②LVM与体重和皮脂厚度均有显著相关性(P<0.05);女性肥胖儿童的体重和皮脂厚度与DmeVG,DaV,DeV／aV均有显著相关性(P<0.05);男性肥胖儿童体重与DaV,皮脂厚度与DaV,DeV／aV有明显相关性(P<0.05);腰臀比与左室肥大和左心功能减低均无相关性(P>0.05)。③LVM与DaV,DeV／aV有明显相关性（P<0.05)。结论 早期的单纯肥胖即出现了左室肥厚和左心功能减低,并与体重和皮脂厚度密切相关。与成人肥胖症不同,肥胖儿童的LVMI无明显改变。腰臀比与心血管系统受累无明显相关性,因儿童期肥胖以周围型肥胖为主。     

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目的了解不同葡萄糖耐量状态的肥胖儿童血清脂联素水平,探讨其与年龄、体重指数(BMI)、血脂、血糖及胰岛素水平的关系。方法选择2002～2004年于广州市儿童医院初诊并住院诊治的肥胖儿童52例,分为36例糖耐量正常(NGT)肥胖组和16例糖耐量受损(IGT)肥胖组。测定两组肥胖儿童和41例年龄、性别匹配的正常儿童空腹血清脂联素、胆固醇(CHO)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDLC)、血糖和胰岛素(FINS),计算胰岛素抵抗指数(HOMAIR)。肥胖组儿童均做口服葡萄糖耐量试验(OGTT),测定OGTT2h血糖和胰岛素。结果正常对照组、NGT肥胖组及IGT肥胖组血清脂联素水平依次降低,HOMAIR依次升高,且均有统计学意义;相关性分析显示肥胖儿童血清脂联素与TG、LDLC、FINS呈显著负相关(P<0.05)。结论肥胖儿童血清脂联素水平降低,并与血脂、胰岛素抵抗密切相关;与NGT肥胖组相比,IGT肥胖组儿童的血清脂联素水平进一步降低。     

瘦素基因多态性与哈萨克族儿童肥胖的关系

目的 探讨瘦素基因型与哈萨克族肥胖儿童的关系.方法 按照肥胖儿童诊断标准,选择乌鲁木齐周边地区96例哈萨克族肥胖患儿(肥胖组)和81例健康对照儿童(非肥胖组),空腹12 h后抽取2组儿童外周静脉血5 mL,常规提取基因组DNA,应用限制性片段长度多态性方法检测其C2549A瘦素基因型,同时检测各组空腹血脂水平,采用放射免疫法测定其空腹血浆瘦素和胰岛素水平.并测量各组儿童身高、体质量.结果 177例受试对象中,AA、AC、CC基因型频率分别为6.8％、52.5％、40.7％.A等位基因频率为33.0％,C等位基因频率为67.0％;瘦素、胰岛素等各项指标在AA+ AC组与CC组间及不同性别间比较差异无统计学意义;肥胖组患儿与非肥胖组儿童比较,除高密度脂蛋白、载脂蛋白A、载脂蛋白B外,其血清三酰甘油、总胆固醇、低密度脂蛋白、瘦素、胰岛素水平肥胖患儿均明显高于非肥胖儿童.结论 在哈萨克族儿童中存在瘦素基因A2549C多态性;瘦素基因多态性与哈萨克族儿童肥胖无关.     

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目的探讨儿童青少年血中胰岛素、瘦素、脂联素和抵抗素水平与肥胖程度的关系。方法选择2004年北京市儿童青少年代谢综合征(BCAMS)调查总样本中的3511例(男1790例,女1721例)6～18岁儿童青少年为研究对象,依据体重指数值分类标准将所有研究对象分为正常体重组1626例、超重组655例和肥胖组1230例。利用酶联免疫吸附试验法(ELISA)检测研究对象空腹血脂肪细胞因子水平。采用协方差分析比较超重组、肥胖组与正常体重组间脂肪细胞因子的差异;不同肥胖程度对预测脂肪细胞因子异常的作用采用多因素Logistic回归分析。结果超重、肥胖组儿童血中胰岛素、瘦素水平高于正常体重组,并随着肥胖程度的增加而升高,且具有明显的男女性别差异;脂联素水平则随着肥胖程度的增加而降低;抵抗素水平仅见肥胖组与正常体重组儿童比较差异有统计学意义。采用多因素Logistic回归模型调整年龄、性别和青春发育期,以正常体重组为参照,进行对比分析。结论儿童青少年血中胰岛素、瘦素、脂联素水平与肥胖程度密切相关,脂肪细胞因子异常检出率随着体重的增加而升高,因此,在儿童青少年时期控制体重、降低肥胖程度对预防儿童成人慢性病至关重要。     

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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。     

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。     

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.     

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目的 探讨β3-肾上腺素能受体基因(p3-AR)Trp64Arg变异与新疆哈萨克族儿童肥胖的相关性.方法 选取乌鲁木齐周边地区95例6-12岁哈萨克族学龄肥胖儿童及87名非肥胖儿童,用限制性片段长度多态性方法检测被调查儿童的基因型,生化方法检测血清甘油三酯(TG)、总胆固醇(TC)、高密度脂蛋白胆固醇(HDLC)、低密度脂蛋白胆固醇(LDL-C)、载脂蛋白A(ApoA)、载脂蛋白B(ApoB)水平,并测量身高、体重.结果 变异型等位基因(C)在被调查对象中出现的频率为0.194,其中男0.210,女0.160.肥胖儿童中变异等位基因(C)、Trp64Arg变异基因型的出现频率明显高于非肥胖者(P＜0.05).单纯性肥胖儿童与非肥胖儿童比较,血清TG、TC、LDL-C、ApoB水平均明显升高(P＜0.05).B3-AR不同基因型间血脂比较,差异无统计学意义(P>0.05).结论 哈萨克族学龄儿童中存在一定的B3-AR Trp64Arg变异,可能与哈萨克族儿童肥胖有关.     

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目的观察二甲双胍治疗对高胰岛素血症肥胖患儿血清脂源性激素脂联素、抵抗素、瘦素水平的影响。方法2004-01—2005-02将武汉市儿童医院和同济医院54例高胰岛素血症肥胖患儿分为轻、中度肥胖组及重度肥胖组,均以二甲双胍治疗12周,测量治疗前后体重、空腹血糖、空腹胰岛素及脂源性激素脂联素、瘦素、抵抗素的变化。结果治疗前轻、中度肥胖组和重度肥胖组高胰岛素血症患儿空腹血糖水平与健康对照组比较差异无显著性(P>0.05),血清胰岛素、瘦素、抵抗素及胰岛素抵抗指数(HOMA-IR)均高于健康对照组(P<0.01),脂联素水平明显低于健康对照组(P<0.01)。二甲双胍治疗12周后与治疗前相比,血清胰岛素水平、胰岛素抵抗指数明显降低(P<0.01),轻、中度肥胖组及重度肥胖组血清瘦素水平分别由治疗前的(24.3±1.8)μg/L、(30.2±5.1)μg/L降低为治疗后的(19.6±6.3)μg/L、(24.7±5.3)μg/L,差异有统计学意义;抵抗素水平分别由治疗前的(16.5±6.0)μg/L、(22.3±5.2)μg/L升高为(22.0±5.1)μg/L、(30.6±11.7)μg/L,差异有统计学意义;轻、中度肥胖组和重度肥胖组血清脂联素水平治疗前分别为(8.4±3.2)mg/L、(6.5±1.2)mg/L,治疗后分别为(8.9±2.3)mg/L、(7.03±3.0)mg/L,治疗前后相比,P>0.05。体重指数(BMI)下降,但差异无显著性。结论二甲双胍能显著改善肥胖患儿胰岛素抵抗。降低血清瘦素水平可能是其改善胰岛素抵抗机制之一,但在对脂源性激素脂联素、抵抗素水平的改善上,有其局限性。     

Insulin and insulin resistance index are not independent determinants for the variation in leptin in obese children and adolescents

Recent findings have questioned the independent influence of insulin on leptin. We studied whether insulin contributes to leptin in obese children, independent of confounding parameters, such as total adiposity, fasting insulin resistance index, and fat free mass. In 100 obese boys and 103 obese girls, blood levels of leptin, insulin, glucose, and triglycerides were determined. The fasting insulin resistance index (FIRI) was calculated, and body composition was assessed by means of impedance. Leptin and glucose were higher in girls, and all estimates of adiposity were significantly associated with leptin. However, when adjusted for adiposity, the relationship between insulin and leptin, and also between FIRI and leptin, remained significant in boys and girls (p<0.05). Although several regression models were tested, neither insulin nor FIRI were found to contribute significantly and independently to leptin. BMI together with triglycerides and FFM were the main determinants for the variation in leptin in boys (adj. R2=0.46, p<0.0001). In girls, BMI explained a great magnitude of the variation in leptin (adj. R2=0.60, p<0.0001). These findings indicate that in the state of childhood and adolescent obesity, total adiposity but not insulin or insulin resistance index is the main determinant for leptin. In contrast to obese girls, the fat free mass and triglycerides contribute significantly to the variation in leptin in obese boys. The biological significance for these findings should be elucidated in longitudinal studies.     

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??Objective??To investigate the correlations between plasma monocyte /macrophage chemoattractant protein and related parameters of insulin resisitance in children with simple obesity. Methods??70 children with simple obesity were enrolled as study group??30 healthy children as control group. Body mass index??BMI ??and waist circumference ??WC??were detected as indices of obesity .Plasma levels of macrophage inflammatory protein-1????MIP-1??????monocyte chemoattractant protein-1??MCP-1 ??were measured by ELISA.The rate of CD68 positive cells in blood were detected by flow cytometry??FCM???? Plasma levels of insulin ??adiponectin were measured by RIA?? Insulin resisitance index ??InRI?? were caculated by homeostasis model assessment of insulin resistance ??HOMA-IR??. The associations between MIP-1????MCP-1 levels and adiponectin and related parameters were analyzed with Pearson correlation analysis or partial correlation analysis??Results??The concentration of MIP-1?? and MCP-1 in plasma in children with simple obesity were higher than that in control group. There was a significant difference between the two groups ??P < 0. 05??. The rate of CD68 positive cells in blood of simple obesity had no significant difference between that in control group ??P > 0.05??.The concentration of MIP-1?? and MCP-1 in plasma had positive correlations with BMI and WC and InRI??P < 0. 05??. The concentration of adiponectin in plasma had negetive correlations with BMI and WC and InRI ??P < 0. 05??. The rate of CD68+ cell in blood had no correlation with BMI and WC and InRI??P < 0. 05??.Conclusion??We found that a differential low-grade inflammation is associated with obesity of children .The levels of MIP-1????MCP-1 in blood of obesity were associated with insulin resistance and abdominal obesity. The levels of plasma MIP-1????MCP-1??adiponectin may predict the onset of obesity related complications.     

Leptin profile in neonatal gonadotropin surge and relationship between leptin and body mass index in early infancy

AIM: This study was designed to investigate the longitudinal and dynamic profile of leptin and its relationship with sex hormones including luteinizing hormone (LH), follicle-stimulating hormone (FSH), estradiol (E2) and testosterone (TTE) in neonatal 'minipuberty'. We also investigated the effects of leptin in the regulation of body weight gain and body mass index (BMI) in the first 3 months of life. METHODS: A longitudinal study was carried out in a cohort of 15 male and 15 female term infants during the first 3 months of life. Blood samples were collected in the morning from the infants on the 3rd, 15th, 30th, and 90th days of life. At each sample collection, anthropometric measurements were recorded. Serum leptin, LH, FSH, E2 (girls only) and TTE (boys only) concentrations were analyzed using standard biochemical methods. Association of leptin with weight gain, BMI, and these hormones during infancy was evaluated. RESULTS: Leptin levels increased significantly between the 3rd and 90th days of life in both boys and girls. BMI of both groups increased significantly from the 3rd to the 90th day. There was no significant difference in the leptin levels and leptin/BMI ratios of the two sexes at different time points. Leptin levels on the 30th and 90th days correlated significantly with BMI in both sexes. LH and FSH levels in both groups were found to be significantly higher on the 15th day of life. No correlation was observed between leptin and LH, FSH, E2 or TTE levels throughout the study. CONCLUSIONS: Leptin levels do not differ between the two sexes during early infancy and possibly there is no role for leptin in the surge of gonadotropins or sex steroids in neonatal minipuberty. The relationship between leptin and BMI could not be seen in the first postnatal days and the transient lack of the regulatory effect of BMI on leptin concentrations might reflect an adaptive resistance in the production of leptin to support catch-up growth after initial physiological weight loss in newborns.