肥胖儿童血清胰岛素水平对体脂分布及胰岛素抵抗和血脂的影响

目的　探讨肥胖儿童血清胰岛素水平与体脂分布、胰岛素抵抗及血脂的关系。方法　对 6 8例单纯性肥胖儿童依据空腹血胰岛素 (FINS)及空腹血糖 (FBG)水平分为高胰岛素血症组 (HIG) 4 3例和正常胰岛素组 (NIG)2 5例 ,测量FBG、胰岛素 (INS)、血脂 ,计算体重指数 (BMI)、腰臀比、稳态模型胰岛素抵抗指数 (HOMA IR)、敏感指数 (HOMA IAI)、胰岛细胞分泌功能 (HOMA IS)及葡萄糖、胰岛素曲线下面积 (AUCBG、AUCINS)。结果　 (1)HIG组BMI、腰围、腰臀比、HOMA IR、HOMA IS、AUCINS明显高于NIG组 (P <0 0 5、0 0 1、0 0 0 1) ,HOMA IAI低于NIG组 (P <0 0 0 1) ;(2 )HIG组FINS与BMI、腰围、腰臀比、HOMA IR、HOMA IS、AUCINS成正相关 (r =0 316 ,0 32 4 ,0 4 6 4 ,0 835 ,0 5 99,0 5 2 5 ,P <0 0 5 ,0 0 5 ,0 0 1,0 0 0 1,0 0 0 1,0 0 0 1) ,与HOMA IAI成负相关(r =- 0 812 ,P <0 0 0 1) ;(3)两组FBG、AUCBG、血脂差异无显著性 (P >0 0 5 )。结论　高胰岛素血症肥胖患儿体内脂质沉积严重且脂肪分布异常 ,胰岛素抵抗更为严重 ,高胰岛素血症可能为肥胖产生的原因之一。     

肥胖儿童血清抵抗素与胰岛素抵抗、β细胞功能的关系

目的研究不同程度肥胖儿童血清抵抗素与胰岛素抵抗(IR)、胰岛β细胞功能的关系。方法根据体质量指数(BMI)将研究对象分为正常对照组(BMI<22,n=30)、肥胖1组(23≤BMI<30,n=82)和肥胖2组(BMI≥30,n=31)。对3组患儿进行葡萄糖耐量试验,测量空腹血清抵抗素,分别采用稳态模型的胰岛素抵抗指数(HOMAIR)、胰岛β细胞功能指数(HOMAβ)和总体胰岛素敏感指数(WBISI)、30min胰岛素增量与葡萄糖增量比值(△I30/△G30)作为基础和糖负荷后胰岛素敏感性和胰岛β细胞功能的评价指标。结果肥胖儿童糖耐量减低6例(5.3%),2型糖尿病2例(1.8%)。随BMI增加,糖负荷后2h血糖(2hPG)、血糖曲线下面积(AUCg)、空腹胰岛素(FINS)、胰岛素曲线下面积(AUCi)和HOMAIR逐步增高(P均<0.05),WBISI逐步降低(P<0.001);肥胖组HOMAβ和△I30/△G30较对照组明显上升(P均<0.05);肥胖组间无显著差异(P均>0.05);空腹血清抵抗素3组间差异无显著性意义(P>0.05);8例糖耐量异常儿童抵抗素较对照组略高,但无显著差异(P>0.05)。BMI与2hPG、FINS、HOMAIR、HOMAβ、△I30/△G30呈明显正相关(P均<0.05),与WBISI呈高度负相关(P<0.001),抵抗素与上述指标及BMI无明显相关(P均>0.05)。结论肥胖儿童存在IR、糖负荷后血糖水平升高和胰岛β细胞分泌功能上调,随肥胖程度加重,胰岛素敏感性进一步降低,而胰岛β细胞分泌功能无相应增强。循环抵抗素水平可能不是介导儿童肥胖及IR的关键因素,抵抗素的确切作用尚待进一步研究。     

儿童青少年代谢综合征与ghrelin基因Leu72Met位点多态性研究

目的探讨儿童青少年代谢综合征（MS）及其组分与胰岛素抵抗（IR）的关系，研究ghrelin基因Leu72Met位点多态性在儿童青少年肥胖症及MS中的作用。方法通过对住院的508例中、重度肥胖青少年的临床研究，计算稳态模型胰岛素抵抗指数（HOMA—IR）及总体胰岛素敏感指数（WBISI）评估IR情况；对其中230例肥胖患儿和100名正常体重儿童青少年，利用PCR、RFLP及基因测序检测ghrelin基因多态性。结果中、重度肥胖儿童青少年MS的发生率为22．83％；HOMA-IR和WBISI两个指标在肥胖组与对照组中差异有统计学意义（P〈0．01），且分别随肥胖程度的增加而升高和下降；与单纯肥胖组比较，伴有代谢组分异常者的HOMA—IR明显增高（P〈0．05），而WBISI显著降低（P〈0．05），且随着代谢组分异常的增多而加重。在儿童青少年中检测到两个ghrelin基因的多态性位点，C214A（Leu72Met）和A269T（Gln90Leu）；肥胖组Leu72Met位点的多态性频率为36．09％，与对照组的41．00％比较差异无统计学意义（P〉0．05）；Gln90Leu在肥胖组和对照组的多态性频率分别为043％和2．00％，差异亦无统计学意义（P〉0．05）；Leu72Met位点各基因型之间比较，年龄、体质指数（BMI）、谷丙转氨酶（ALT）、甘油三酯（TG）、总胆固醇（TC）、WBISI差异均无统计学意义。结论肥胖儿童青少年存在IR，且随肥胖程度及MS各代谢组分异常增加而加重；Leu72Met位点的多态性改变与汉族儿童青少年肥胖及MS的发生无关。     

循环Alarin在肥胖儿童中的水平及与胰岛素抵抗的相关性

目的 本研究拟探讨循环Alarin在肥胖儿童中的表达水平及与代谢参数的关系。方法 招募体重指数（BMI）高于第95百分位数的肥胖儿童86例为肥胖组,82例年龄和性别与肥胖组匹配的BMI低于第85百分位数的健康儿童作为健康对照组。根据是否发生胰岛素抵抗（IR）,将86例肥胖组儿童分为IR组（n=27）和非IR组（n=59）。测量身高、体重、收缩压（SBP）和舒张压（SDP）,并计算体重指数（BMI）。检测总胆固醇（TC）、甘油三酯（TG）、低密度脂蛋白胆固醇（LDL-C）、高密度脂蛋白胆固醇（HDL-C）、尿酸（UA）、空腹胰岛素（FINS）及空腹血糖（FBG）水平,并计算葡萄糖和胰岛素曲线下面积（AUC）、稳态模型胰岛素抵抗指数（HOMA-IR）、全身胰岛素敏感性指标（WBISI）。ELISA法检测循环Alarin水平。结果 肥胖组儿童循环Alarin水平较健康对照组显著升高,IR组儿童循环Alarin水平较非IR组显著升高（P < 0.01）。循环Alarin与BMI、TG、FBG、AUC_葡萄糖、AUC_胰岛素、HOMA-IR呈正相关,与WBISI呈负相关（P < 0.05）。循环Alarin的变化与BMI、FBG、HOMA-IR有线性回归关系,其中HOMA-IR对循环Alarin的影响最大（P < 0.05）。结论 循环Alarin水平在肥胖儿童中显著升高,可能与肥胖和IR的发生有关。     

肥胖儿童非酒精性脂肪肝炎54例

目的 观察不同程度肥胖儿童非酒精性脂肪肝炎(NASH)的发病状况,探讨其可能的发病机制.方法 体质量指数(BMI)≥23的7～16岁单纯性肥胖儿童123例.按BMI分为3组:BMI≥30组34例,25≤BMI＜30组57例,23≤BMI＜25组32例.分别进行肝脏B超检查,并检测血转氨酶、胆固醇、三酰甘油(TG)及空腹血糖/空腹胰岛素比值(FlGIR).将另24例仅有肥胖而无肝脂肪病变者设为对照组.结果 123例患儿中B超发现肝脂肪病变99例(80.49%),其中符合NASH诊断标准者54例(43.90%).所有患儿中,BMI≥30组脂肪肝炎及FGIR＜7的发生率均显著高于其他2组(Pa ＜0.01).相关分析表明,ALT和AST与BMI分级、血胆固醇、TG、FGIR均有相关性(r=0.413,0.290,0.379,-0.477 Pa ＜0.01;r=0.359,0.349,0.348,-0.369 Pa ＜0,01).NASH患儿与对照组血脂、FGIR、BMI比较差异均有统计学意义(X2=9.84,25.59 Pa ＜0.01;t=5.05P＜0.01).结论 BMI ≥30是肥胖儿童发生NASH的高危因素,且脂代谢紊乱和胰岛素抵抗可能与其发病有关.     

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。     

口服葡萄糖耐量试验对肥胖代谢综合征患儿的诊断价值

目的 探讨肥胖儿童口服葡萄糖耐量试验(OGTT)及胰岛素释放试验中血糖、胰岛素水平与胰岛素抵抗的关系,评价其在代谢综合征(MS)诊断中的价值.方法 2006年3月-2008年3月于本科内分泌门诊就诊的肥胖儿童100例,分为MS组56例和非MS组44例.2组均行人体测量,并取血测血脂,行OGTT和胰岛素释放试验.稳态模型评估法(HOMA)计算胰岛素抵抗指数(HOMAIR)、胰岛素分泌指数(HOMAIS)、总体胰岛素敏感指数(WBISI).通过ROC曲线判断试验诊断价值, 选择Youden指数最大值为最佳临界点.结果 1.各个时间点的血糖、胰岛素水平均与WBISI相关,而且同一时间点胰岛素较血糖的相关性更强.MS组HOMAIR高于非MS组,WBISI低于非MS组,差异有统计学意义(Pa<0.01),2组间HOMAIS无差别.2.在不包括糖尿病及糖耐量减低儿童中服糖后60 min血糖、胰岛素水平对预测MS有价值,以血糖6.5 mmol/L,胰岛素120 mU/L为临界点时敏感性分别为0.636、0.660,特异性分别为0.667、0.632,同时存在时敏感性可达0.775,特异性达到0.689.结论 OGTT和胰岛素释放试验中各个时间点血糖、胰岛素水平不仅对糖代谢异常有诊断意义,且对预测糖代谢尚未见异常的肥胖儿童MS有重要意义.     

非酒精性脂肪肝炎患儿脂代谢紊乱及胰岛素抵抗研究

目的　探讨非酒精性脂肪肝炎(NASH)与脂代谢紊乱及胰岛素抵抗之间的关系。方法　对2 0 0 3年6～1 0月浙江大学医学院附属儿童医院收集的54例诊断为NASH的肥胖儿童及2 4例既无脂肪肝影像学改变也无肝转氨酶升高的单纯性肥胖儿童(对照组) ,进行血甘油三酯、胆固醇、空腹血糖/空腹血胰岛素比值(FGIR)的检测,分析NASH与高脂血症和胰岛素抵抗之间的关系。并对其中2 0例怀疑合并良性黑棘皮病的患儿行皮肤病理活检以确诊,分析NASH与良性黑棘皮病的关系。结果　54例NASH的患儿体重指数(BMI)为( 2 8 .1 0±4 .1 6) ,对照组BMI为( 2 3 . 91±1 . 88) ,二者相比,差异有显著性意义(t=5. 0 5,P <0 .0 1 )。NASH组中高脂血症及胰岛素抵抗(FGIR <7)的发生率分别为59. 2 6%和70 . 3 7% ,明显高于对照组(发生率为2 0 .83 % ,8 3 .3 % ,χ2 =9. 84,χ2 =2 5. 59,P <0 . 0 1 )。经相关分析,发现丙氨酸转氨酶(ALT)及天冬氨酸转氨酶(AST)与BMI、血胆固醇、血甘油三酯、FGIR呈显著相关(rs=0 . 41 3 ,0 . 2 9,0 . 3 79,-0 . 477,P <0 . 0 1 ;rs=0 . 3 590 3 4 .9,0 .3 4 8,-0 . 3 69,P <0. 0 1 )。且其中2 0例伴良性黑棘皮病(占3 7. 0 4% )。结论　NASH患儿存在严重的脂代谢紊乱及胰岛素抵抗。约1 /3以上NASH患儿合并良性     

单纯性肥胖患儿非酒精性脂肪肝病与胰岛素抵抗

目的探讨单纯性肥胖(肥胖)儿童发生非酒精性脂肪肝病(NAFLD)的情况及与胰岛素抵抗(IR)、血脂、体质量指数(BMI)、腰臀比(WHR)的关系。方法选择肥胖儿童90例,年龄2.5～14.3岁。其中NAFLD 24例(NAFLD组),无NAFLD 66例(无NAFLD组)。另选35例年龄、性别与其相匹配的健康儿童为健康对照组。清晨空腹测量其体质量、身高、腰围和臀围,计算BMI和WHR,同时静脉采血检测其血清胰岛素(FINS)、糖(FBG)、胆固醇(TC)、三酰甘油(TG)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)和ALT、AST等,计算稳态模型胰岛素抵抗指数(HOMA-IR=FINS×FBG/22.5),并做肝胆等部位超声检查。结果 NAFLD占肥胖儿童的26.67%;NAFLD组儿童BMI、WHR最高,其次为无NAFLD组,差异均有统计学意义(Pa<0.001);3组儿童FINS和HOMA-IR值差异均有统计学意义(Pa<0.001),NAFLD组最高,其次为无NAFLD组,均明显高于健康对照组,但FBG无明显差异;NAFLD组血清TG、LDL-C和TC水平明显高于无NAFLD组和健康对照组(Pa<0.01);HOMA-IR值与BMI、WHR、血TG、LDL-C呈正相关(r=0.402、0.256、0.239、0.180,P=0.000、0.004、0.008、0.046);BMI、WHR诊断NAFLD的受试者工作特征(ROC)曲线下面积分别为0.805和0.765(Pa=0.000)。结论肥胖儿童NAFLD的发生与IR,血TG、LDL-C、TC升高及BMI、WHR增高关系密切,BMI、WHR对儿童肥胖NAFLD具有一定的诊断价值。控制体质量,减少腰围,可减轻IR,阻止NAFLD的发生、发展。     

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目的分析中枢性性早熟(CPP)女童糖脂代谢的特点及脂联素在性早熟女童糖、脂代谢中的作用。方法浙江大学医学院附属儿童医院于2004年6~10月收治50例CPP女童,测量空腹血糖、胰岛素、甘油三酯、胆固醇、脂联素,并做葡萄糖耐量试验和胰岛素释放试验,采用总体胰岛素敏感指数(WBISI)、胰岛素抵抗指数(HOMA-IR)这2个指标来评估胰岛素敏感性和胰岛β细胞功能。并与年龄匹配的正常对照组进行比较。结果(1)CPP女童空腹胰岛素、HOMA-IR明显高于正常对照组(P<0·01)。(2)CPP女童A1组胆固醇较正常对照组明显升高(P<0·05)。(3)CPP女童体重指数(BMI)值均较正常对照组明显升高(P<0·05)。其中超重16%(8/50),肥胖8%(4/50)。(4)CPP女童脂联素均较正常对照组明显下降(P<0·01)。(5)CPP女童BMI值与WBISI显著负相关(r=-0·31,P<0·05),与HOMA-IR显著正相关(r=0·30,P<0·05),与脂联素显著负相关(r=-0·43,P<0·01)。CPP女童脂联素与WBISI显著正相关(r=0·29,P<0·05),多元回归分析显示CPP女童脂联素与WBISI、HOMA-IR无显著相关性。(6)排除12例超重加肥胖CPP女童后再分析显示A1、A2组女童空腹胰岛素、HOMA-IR仍明显高于正常对照组(P<0·01),而脂联素水平3组差异无显著性。结论(1)CPP女童存在不同程度的胰岛素抵抗,尤见于BMI值明显升高的性早熟女童。(2)肥胖或超重的性早熟女童胰岛素抵抗可能与脂联素水平下降有关。     

肥胖儿童非酒精性脂肪肝病及代谢综合征发病情况分析

目的 研究肥胖儿童中非酒精性脂肪肝病(NAFLD)与代谢综合征(MS)的发生情况,并探索两者之间的关系.方法 对308例在本院内分泌科住院的9～14岁肥胖儿童进行腰围、体块指数、血脂、肝功能、肝脏B超、糖耐量试验及胰岛素释放试验等各项检查,根据诊断标准分别计算发生NAFLD[包括单纯性非酒精性脂肪肝(SNAFL)、非酒精性脂肪肝炎(NASH)]和MS的患病率,并将308例肥胖患儿分为无肝脏损害的肥胖儿童组(OCWLD组),SNAFL组和NASH组,比较各组胰岛素、胰岛素抵抗(IR)指标及MS的发病率和MS组成成分的发病率.结果 (1)308例中发生NAFLD的达到203例(65.9%),其中发生SNAFL者140例(45.5%),发生NASH者63例(20.5%).(2)308例中发生MS 76例(24.7%),这76例中合并有NAFLD的64例(84.2%).NAFLD组中MS 64例(31.5%),高于OCWLD组的12例(11.4%),差异有统计学意义,但SNAFL组中MS 41例(29.3%),与NASH组的23例(36.5%)比较差异无统计学意义.(3)就单个MS的组成成分来说,OCWLD组与SNALF组比较仅在高血压的发病率上差异有统计学意义,而OCWLD组与NASH组比较在高血压、高血脂、高血糖的发病率上差异均有统计学意义;SNALF组与NASH组比较在高血脂的发病率上差异有统计学意义.随OCWLD向SNAFL和NASH发展,空腹胰岛素水平逐渐上升,IR也越加明显.但NAFLD患儿与MS患儿比较各IR指标差异无统计学意义.结论 肥胖儿童中NAFLD和MS的发生率均已相当高,MS患儿合并NAFLD的比例很高,IR是NAFLD和MS共同的发病基础,且随着NAFLD患儿病情的进展,MS成分指标越来越严重,IR也越来越严重.     

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。     

Assessment of insulin sensitivity from measurements in fasting state and during an oral glucose tolerance test in obese children

BACKGROUND: Few previous studies have examined the validity of the fasting glucose-to-insulin ratio (FGIR), homeostasis model assessment of insulin resistance (HOMA-IR) and quantitative insulin-sensitivity check index (QUICKI) in pediatric populations. OBJECTIVE: To compare simple indices of insulin resistance calculated from fasting glucose and insulin levels with insulin sensitivity indices (area under the response curve [AUCinsulin], insulin sensitivity index [ISI-compositeL) determined by oral glucose tolerance testing (OGTT) in obese children. METHODS: One hundred and forty-eight obese children and adolescents (86 girls and 62 boys, mean age: 10.86 +/- 3.08 years, mean body mass index (BMI): 27.7 +/- 4.2) participated in the study. OGTT was performed in all participants. After glucose and insulin measurements from OGTT, the children were divided into two groups according to the presence or absence of insulin resistance. Insulin sensitivity indices obtained from the OGTT were compared between the groups. The total plasma glucose response and insulin secretion were evaluated from the AUC estimated by the trapezoid rule. Cut-off points, and sensitivity and specificity calculations were based on insulin resistance with receiver operating characteristic curve (ROC) analysis. RESULTS: The prevalence of insulin resistance, glucose intolerance and dyslipidemia was 37.1%, 24.3% and 54% in obese children, respectively. The groups consisted of 93 children without insulin resistance (54 girls and 39 boys; mean age: 10.5 +/- 3.3 years; mean BMI: 27.0 +/- 4.2) and 55 children with insulin resistance (32 girls and 23 boys; mean age: 11.4 +/- 2.5 years; mean BMI: 27.9 +/- 3.9). There were significant differences in mean FGIR (10.0 +/- 7.2 vs 5.6 +/- 2.8, p < 0.001), HOMA-IR (3.2 +/- 2.3 vs 4.9 +/- 2.3, p < 0.001) and QUICKI (0.33 +/- 0.03 vs 0.30 +/- 0.02, p < 0.001) between the groups. The cut-off points for diagnosis of insulin resistance were < 5.6 for FGIR (sensitivity 61.8, specificity 76.3), > 2.7 for HOMA-IR (sensitivity 80, specificity 59.1), and < 0.328 for QUICKI (sensitivity 80, specificity 60.2). CONCLUSIONS: Indices derived from fasting samples for diagnosis of insulin sensitivity are reliable criteria in obese children and adolescents. HOMA-IR and QUICKI appeared to have similar sensitivity and specificity and to have higher sensitivity than FGIR.     

Prevalence of type 2 diabetes mellitus and impaired glucose tolerance in obese Argentinean children and adolescents

The aim of this study was to evaluate the prevalence of type 2 diabetes mellitus (DM2) and impaired glucose tolerance (IGT) in obese children and adolescents and to examine insulin resistance and insulin secretion. We studied 427 asymptomatic obese patients. DM2 and IGT were diagnosed by an oral glucose tolerance test. Insulin resistance and P-cell function were assessed by using homeostasis model assessment (HOMA), insulin/glucose index (I/GI), fasting insulin and insulin sensitivity index (ISI-composite). Thirty patients showed IGT (7%) and seven had DM2 (1.6%). The mean age was 10.7 +/- 3.5 years, the diabetic group being significantly older than the normal group (p < 0.01). The mean body mass index was 30 +/- 5.3 kg/m2 without significant differences between groups. beta-Cell function declined significantly in the patients with IGT and DM2, and insulin resistance increased significantly. Given the rather high prevalence of glucose metabolism impairment, children with obesity should undergo glucose tolerance testing for appropriate therapeutic intervention.     

非酒精性脂肪性肝病儿童血清TIMP-1和TIMP-2检测及临床意义

目的：了解非酒精性脂肪性肝病患儿基质金属蛋白酶组织抑制物（TIMP）-1和TIMP-2的水平及价值。方法根据诊断标准将105例肥胖儿童分为单纯性肥胖（n=44）、单纯性非酒精性脂肪肝（SNAFL,n=25）和非酒精性脂肪肝炎（NASH,n=36）3组,采用酶联免疫吸附方法(ELISA)测定血清TIMP-1、TIMP-2,全自动酶法测定丙氨酸氨基转移酶(ALT)和γ-谷氨酸转肽酶(γ-GT)。结果随着单纯性肥胖向SNAFL和NASH发展,TIMP-1和γ-GT水平逐步升高,差异有统计学意义(P0.05)。结论 血清TIMP-1和TIMP-2指标均可不同程度地反映肝脏的纤维化程度,其中以TIMP-1更为可靠、有效。［中国当代儿科杂志,2010,12（6）：455-458］     

Serum levels of soluble tumor necrosis factor-alpha receptor 2 are linked to insulin resistance and glucose intolerance in children

BACKGROUND: Obesity and insulin resistance are increasingly common problems in children. Tumor necrosis factor-alpha (TNF-alpha) has important effects on lipid and glucose metabolism. This effect may be mediated through soluble TNF-alpha receptor 2 (sTNFR2). OBJECTIVE: To investigate the relationship between insulin resistance and the TNF-alpha system in childhood obesity. CHILDREN AND METHODS: Twenty-one obese and six non-obese children were studied. Body mass index (BMI) z-scores, percent body fat (PBF) and waist to hip ratio (WHR) were determined. Fasting serum levels of total cholesterol, HDL-cholesterol, LDL-cholesterol, TNF-alpha and sTNFR2 were measured. A standard 2-hour oral glucose tolerance test (dose of glucose: 1.75 g/kg, max. 75 g) was done. Insulin resistance (IR) was estimated by fasting plasma insulin, plasma insulin at 120 min, homeostasis model assessment (HOMA) and insulin area under the curve (AUC) from OGTT. Insulin sensitivity was estimated by oral glucose insulin sensitivity (OGIS120). RESULTS: Among the obese participants, one child (5.2%) was found to have diabetes mellitus and four others (21.1%) impaired glucose tolerance (IGT). Obese children had significantly elevated sTNFR2 levels. Furthermore, the group of obese children with IGT and the patient with newly diagnosed diabetes mellitus together (n = 5) had significantly higher levels of serum sTNFR2 (2,865+/-320 pg/ml) than the rest of the obese (2,460+/-352 pg/ml; p = 0.016) or lean (1,969+/-362 pg/ml; p = 0.014) children. Serum sTNFR2 levels correlated positively with insulin AUC, HOMA IR, fasting plasma insulin, plasma insulin at 120 min, total cholesterol and LDL/ HDL ratio, and negatively with OGIS120. Multiple regression analysis revealed that age, WHR, sTNFR2 and LDL predicted 81% of the variability in glucose at 120 min. CONCLUSION: sTNFR2 is a candidate marker of insulin resistance and glucose intolerance.     

Fatty Liver Disease in Children—What Should One Do?

The world’s population is increasingly overweight and obese. According to the World Health Organization (WHO) as of 2010, 43 million children under the age of five were overweight. Once considered to be limited to developed countries, overweight and obese children are now found in low- and middle-income countries, though most commonly in urban areas. Furthermore the WHO now cites the conditions of overweight and obesity as being associated with more deaths around the globe than those associated with being underweight. With this increased prevalence of overweight and obese children has come a host of other medical problems including nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH). This review will focus on NAFLD and NASH, their definitions, epidemiology, diagnosis and treatment. The authors will also discuss NAFLD in the Indian subcontinent, and the future of NAFLD and NASH.     

Insulin resistance and hyperinsulinemia in prepubertal obese children

BACKGROUND: Tissue resistance to insulin has been demonstrated in obese individuals. Pancreatic beta-cells respond to the reduced tissue sensitivity with increased insulin secretion so that glucose homeostasis is maintained. OBJECTIVE: The purpose of this prospective study was to investigate the presence of hyperinsulinemia and insulin resistance in obese children and adolescents. SUBJECTS AND METHODS: Fasting glucose (FG) and insulin (FI) levels and fasting glucose to insulin ratio (FGIR) were measured in 26 obese prepubertal children and 20 obese adolescents, as compared to 20 non-obese prepupertal children and 20 adolescents with normal body weight. Furthermore, obese children and adolescents underwent an oral glucose tolerance test with measurements of glucose and insulin 2 hours post glucose load. RESULTS: In 14/26 (54%) obese prepubertal children and in 16/20 (80%) obese adolescents FI was >24 microU/ml. FGIR was <6 in 23/26 (88%) prepubertal obese children and in all obese adolescents. All non-obese prepubertal children and adolescents had normal FI. However, FGIR was <6 in 6/20 (30%) non-obese prepubertal children and in 15/20 (75%) non-obese adolescents. CONCLUSION: Hyperinsulinemia and insulin resistance are already present in prepubertal obese children. As hyperinsulinemia is a potentially reversible condition and the complications related to it may be prevented, early measurements should be undertaken so that obese children lose body weight before the onset of puberty which may enhance the problem of insulin insensitivity.     

单纯性肥胖儿童黑色棘皮症与胰岛素抵抗性及细胞因子的关系

目的 探讨单纯性肥胖儿童的黑色棘皮症(AN)和体质量指数、胰岛素抵抗性、瘦素、血浆酶原纤维蛋白溶解原活化抑制剂(PAI-1)的关系。方法 单纯性肥胖儿童38例,其中AN阳性17例,测量身高、体质量、腹围、臀围,同时测血胰岛素、瘦素、空腹血糖、PAI-1。结果 AN阳性者肥胖度、腹围、空腹胰岛素、自动动态平衡标准评价胰岛素抵抗指数(HOMA-R)关系有显著差异,AN与体脂肪率间无关。AN阳性肥胖儿中均升高,PAI-1 40μg／L以上,瘦素30 μg／L以上者均为AN阳性。结论　单纯性肥胖儿童,特别是伴AN阳性肥胖儿,要特别注意随访观察2型糖尿病和冠状动脉疾病的发生和发展。     

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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。