FTO基因SNP rs9939609, rs1421085多态性与儿童青少年肥胖及其代谢指标的相关性研究

目的 研究FTO(fat-mass and obesity associated)基因SNP rs9939609和rs1421085多态性与儿童青少年单纯性肥胖及其代谢指标的相关性。方法 以2004至2006年于复旦大学附属儿科医院内分泌门诊就诊的汉族单纯性肥胖和超重儿童青少年分别作为肥胖组和超重组;选择上海市某中学正常体重汉族学生作为正常对照组。分别测量身高和体重,计算BMI。测定血清空腹葡萄糖（FPG）、空腹胰岛素(FIns)、三酰甘油(TG)和总胆固醇(TC)水平。计算胰岛素抵抗指数（HOMA-IR）和胰岛素敏感指数（QUICKI）。抽提外周血基因组DNA,采用Taqman-MGB探针技术检测FTO基因SNP rs9939609和rs1421085多态性,分析不同基因型与代谢指标和BMI的相关性。结果 肥胖组纳入236例,超重组纳入239例,正常对照组纳入241名。①肥胖+超重组的BMI、FPG、FIns、TG和 HOMA-IR显著高于正常对照组;②肥胖、超重和正常对照组rs9939609分型成功率分别为94.9%（224/236例）、97.9（234/239例）和95.9%（231/241名）,rs1421085分型成功率分别为92.8%（219/236例）、97.1% （232/239例）和95.4%（230/241名）。rs9939609 AA基因型频率：肥胖组为2.7%,超重组为0.4%,正常对照组为1.7%,肥胖+超重组A等位基因频率显著高于正常对照组（OR=1.437,P=0.048）;rs1421085 CC基因型频率：肥胖组为2.7%,超重组为0.9%,正常对照组为1.7%,肥胖+超重组C等位基因频率高于正常对照组,但差异无统计学意义（OR=1.388,P=0.076 0）;③rs1421085 TC +CC基因型和rs9939609 TA +AA 基因型儿童青少年的BMI显著高于TT基因型（rs9939609：P=0.000 3;rs1421085：P=0.000 5）;rs1421085 TC +CC基因型和rs9939609 TA +AA 基因型与FPG、FIns、TG、TC、HOMA-IR、QUICKI无显著相关性。结论 FTO基因SNP rs9939609和rs1421085多态性与中国汉族儿童青少年肥胖和（或）超重存在相关性。A等位基因频率远低于欧洲人群,对BMI的作用效果与欧洲人群相似,但对代谢指标影响存在显著差异。     

脂联素基因SNP276多态性与儿童青少年肥胖的相关性研究

目的研究脂联素（APM1）基因SNP276 G/T多态性与儿童青少年单纯性肥胖及其代谢指标的相关性。方法以2004至2006年于复旦大学附属儿科医院内分泌门诊就诊的单纯性肥胖或超重儿童青少年分别作为肥胖组和超重组;选择某中学正常体重学生作为正常对照组。分别测量身高和体重,计算体重指数（BMI）。测定血清空腹葡萄糖（FPG）、空腹胰岛素(FIns)、三酰甘油(TG)和总胆固醇(TC)水平。计算胰岛素抵抗指数（HOMA-IR）和胰岛素敏感指数（QUICKI）。抽提外周血基因组DNA,采用Taqman-MGB探针技术检测APM1基因SNP276 G/T多态性,分析不同基因型与代谢指标和BMI间的关联性。 结果肥胖组纳入227例,超重组纳入231例,正常对照组纳入216名。①肥胖+超重组的BMI、FPG、FIns、TG和HOMA-IR均显著高于正常对照组。②基因分布频率符合Hardy-Weinberg平衡。③肥胖组、超重组和正常对照组的G等位基因频率分别为71.4％、72.5％和69.7％,GG基因型频率分别为50.2％、52.4％和45.8％,GT基因型频率分别为42.3％、40.3％和47.7％;各组差异均无统计学意义（P均>0.05）。 ④SNP276 GG、GT和TT基因型的BMI、FPG、FIns、TG、TC、HOMA-IR和QUICKI差异均无统计学意义（P＝0.49~0.99）。⑤肥胖+超重组IFG儿童青少年中GG+GT型有70例,TT型4例;正常对照组IFG儿童青少年中GG+GT型有10例,TT型0例;两组差异无统计学意义（P＝0.45）。结论APM1基因SNP276 G/T多态性与青少年儿童单纯性肥胖及其代谢指标间无显著关联性,提示该SNP位点可能存在种族特异性。     

配对盒 4 基因 R192S、R192H 多态性与儿童青少年肥胖的研究

目的研究配对盒4(PAX4)基因rs3824004(574CA;R192S)、rs2233580(575GA;R192H)多态性与儿童青少年肥胖及代谢指标的相关性。方法随机选取103例肥胖儿童,平均年龄(10.82±2.57)岁,体质指数(BMI)(26.82±4.57)kg/m2;同期体检的100例正常体质量儿童为对照组,年龄(10.60±2.84)岁,BMI(16.79±2.13)kg/m2。测量并比较两组血压、体格指标以及血代谢指标。肥胖组儿童行口服葡萄糖耐量试验(OGTT)和胰岛素释放试验,计算稳态模型胰岛素抵抗指数(HOMA-IR)和总体胰岛素敏感指数(WBISI)。应用聚合酶链反应(PCR)检测PAX4 rs3824004、rs 2233580多态性,分析多态位点的等位基因频率和基因型频率及组间差异,以及不同基因型与代谢指标的相关性。结果肥胖组的身高、体质量、BMI、收缩压、舒张压、腰围、臀围、腰围身高比(WHt R)、空腹血糖(FPG)、总胆固醇(TC)、低密度脂蛋白(LDL)、三酰甘油(TG)、丙氨酸转氨酶(ALT)及天冬氨酸转氨酶(AST)均高于对照组,高密度脂蛋白(HDL)低于对照组;差异均有统计学意义(P0.05)。基因分布频率符合Hard-Weinberg平衡,rs3824004肥胖组和对照组的A等位基因频率分别为4.9%和5.0%,CA基因型频率分别为9.7%和10.0%;两组差异均无统计学意义(P0.05)。rs 2233580肥胖组的GA基因型频率为25.2%,高于对照组(11.0%);A等位基因频率为12.6%,也高于对照组(5.5%),差异均有统计学意义(P0.05)。rs2233580 GA基因型的BMI及腰围高于GG基因型,差异均有统计学意义(P0.05),但logistic回归分析显示PAX 4 rs 2233580基因型与代谢指标并无相关性(P均0.05)。肥胖组PAX 4 rs 2233580不同基因型间HOMA-IR和WBISI差异无统计学意义(P均0.05)。结论 PAX 4 rs 2233580影响BMI及腰围,可能参与儿童肥胖的发生,但不是儿童青少年肥胖发生的独立影响因素。     

脂联素基因多态性变化与儿童单纯性肥胖的关系

目的：分析长沙市区儿童脂联素基因+45 位点单核苷酸多态性（SNP）基因型的分布频率,探讨其与儿童肥胖症的相关性。方法：随机抽取147例肥胖儿童及 118 例健康儿童,采用聚合酶链反应-限制性片段长度多态性（PCR-RFLP）方法检测脂联素基因 SNP+45 多态性位点、双抗体夹心 ELISA 测定血清脂联素。同时进行腰围（WC）、腰臀比（WHR）、体脂百分比（%BF）、收缩压（SBP）、舒张压（DBP）、空腹血糖（FPG）、血清甘油三酯（TG）、总胆固醇（TC）、高密度脂蛋白胆固醇（HDL-C）、低密度脂蛋白胆固醇（LDL-C）、空腹胰岛素水平（FINS）、稳态模型胰岛素抵抗指数（HOMA-IR）的测定。结果：肥胖组和正常组的SNP + 45 多态性发生频率分别为 40.5% 和 25.4%,两组间基因型分布与等位基因频率差异均有统计学意义（P<0.05）。肥胖儿童中,TT 基因型与 TG、GG 型相比,其脂联素水平高,而 %BF、HOMA-IR、TC 和 LDL-C 水平低,差异有统计学意义（P<0.05）。结论：脂联素基因SNP+45 变异可能与儿童单纯性肥胖相关,T→G 突变可增加儿童肥胖症的发生,同时使脂联素水平下降。     

不完全川崎病患儿遗传易感性研究

目的 分析2 个与川崎病(Kawasaki disease, KD)相关的基因CD40 基因及BLK 基因位点在不完全KD 中的单核苷酸多态性(SNP)分布特点,并探讨其与不完全KD 的遗传易感性以及临床表型的相关性。方法 采用病例对照研究方法,选取184 例不完全KD 患儿和203 例体检正常儿童作为研究对象。利用限制性片段长度多态性分析的方法测定CD40 基因及BLK 基因SNP 位点多态性分布,比较两组其SNP 位点基因型分布,并分析其基因多态性与不完全KD 临床特点的相关性。结果 患儿CD40 基因SNP 位点(rs1569723)的3 种基因型(AA,AC,CC)频率及等位基因频率与对照组相比差异均无统计学意义。BLK 基因SNP 位点(rs2736340)的基因型频率与对照组相比差异有统计学意义(P=0.031),且KD 组T 等位基因频率明显高于对照组(P=0.007)。CD40 基因SNP 位点(rs1569723)3 种不同基因型患儿结膜充血的比例差异有统计学意义(P=0.036);而BLK基因中SNP 位点(rs2736340)的多态性与患儿四肢末端改变相关(P=0.017)。结论 BLK 基因SNP 位点(rs2736340)与不完全KD 的易感性相关;BLK 基因SNP 位点(rs2736340)及CD40 基因SNP 位点(rs1569723)多态性与部分临床表型相关。     

SLC26A9基因多态性与儿童哮喘相关性分析

目的探讨我国中部地区汉族儿童中SLC26A9基因SNP位点(rs2282430和rs12031234)多态性与哮喘及其临床特点的关系。方法利用病例对照的研究方法,选取203例哮喘患儿和221例健康儿童为研究对象,利用限制性片段长度多态性分析(PCR-RFLP)的方法检测两个SNP位点多态性,并进行统计分析。结果哮喘患儿与对照组之间,SNP位点rs2282430的3种基因型(AA、AG、GG)分布差异有统计学意义(P=0.042),哮喘患儿AA基因型的比例较高;在隐性模式下(AA对AG+GG),两组相比差异有统计学意义(P=0.028)。哮喘患儿SNP位点rs2282430的A等位基因频率高于对照儿童,差异有统计学意义(P=0.011),提示A等位基因为风险因子。而哮喘患儿与对照组儿童之间,SNP位点rs12031234的3种基因型(TT、GT、GG)分布差异无统计学意义(P=0.479),等位基因频率差异也无统计学意义(P=0.215)。哮喘患儿SNP位点rs2282430不同基因型之间,淋巴细胞总数、中性粒细胞百分比、C反应蛋白、免疫球蛋白E、以及嗜酸性粒细胞百分比的差异均无统计学意义(P0.05)。结论 SLC26A9基因SNP位点rs2282430的多态性与我国中部地区儿童哮喘的易感性相关;但该位点的多态性与LYM、CRP、Ig E、NEU%以及EOS%等指标不具有相关性。     

MPO基因多态性与川崎病及其临床表型的相关性分析

目的探讨我国中部汉族人群中MPO基因的单核苷酸多态性(SNP)位点(rs2333227,—643G/A)多态性与川崎病(KD)及其临床特点的相关性。方法采用病例对照研究方法,选取237例典型KD患儿和249例正常儿童作为研究对象。利用PCR-RFLP的方法测定SNP位点多态性分布;并收集KD患儿临床资料。结果 KD患儿SNP位点(rs2333227)的基因型(GG、GA、AA)频率与正常儿童相比差异有统计学意义(P=0.039),且等位基因频率差异亦存在统计学意义(P=0.012),G等位基因为风险因子。该SNP位点GG基因型的患儿手足水肿的比例高于其他基因型的患儿,差异具有统计学意义(P=0.029)并与腹腔积液的特点相关(P=0.028);该SNP位点多态性与结膜充血、皮疹、冠状动脉损伤肝脏肿大、脾脏肿大、小叶性肺炎等影像学特点无关(P0.05)。结论 MPO基因SNP位点(rs2333227)与KD的易感性相关,G等位基因为风险因子;且该SNP位点多态性可能与部分临床特点相关。     

FTO基因rs9939609位点多态性与儿童肥胖的相关性研究

目的探讨不同程度肥胖儿童的生化指标和脂肪含量与肥胖相关基因(FTO)rs9936609单核苷酸多态性位点(SNP)之间的相关性。方法纳入153例7~11岁儿童,其中肥胖102例、超重51例作为研究对象;160例正常体质量儿作为正常对照组。检测并比较各组间肝功能及其他生化指标的差异;利用PCR直接测序法检测FTO基因rs9939609的SNP,计算等位基因分布频率。结果 FTO基因rs9939609 TT、TA/AA基因型在肥胖、超重和正常三组间的分布差异有统计学意义(χ2=23.01,P0.001);其中肥胖组和超重组TA/AA基因型表达频率均分别高于对照组,差异有统计学意义(P’0.014)。T、A等位基因在正常对照组、超重组和肥胖组的频率分别为96.25%和3.75%,85.29%和14.71%,85.78%和14.22%,三组间的分布差异有统计学意义(χ2=21.72,P0.001);肥胖组和超重组A等位基因频率均分别高于对照组,差异有统计学意义(P’0.014)。TA、AA基因型携带者体质指数(BMI)高于TT型携带者,差异有统计学意义(P0.05)。结论 FTO基因rs9939609多态性和儿童肥胖的发生与发展有相关性,A等位基因可导致携带者BMI升高。     

Shank3基因单核苷酸多态性与中国汉族儿童孤独症的关联

目的 探讨Shank3基因单核苷酸多态性(SNPs)与中国汉族儿童孤独症之间的关系.方法 采用PCR与限制性片段长度多态性(PCR-RFLP)分析方法对82例孤独症儿童及80例健康儿童Shank3基因上的2个SNPs位点rs9616915和rs13057681的基因型和等位基因进行测定.采用病例-对照方法分析SNPs位点等位基因的分布,对孤独症组和健康对照组SNPs位点进行Hardy-Weinberg平衡检验.结果 1.健康对照组和孤独症组儿童观察值和预期值间差异均无统计学意义(Pa>0.05),即健康对照组和孤独症组均符合Hardy-Weinberg遗传平衡法则.2.二组儿童rs9616915和rs13057681位点等位基因频率和基因型分布上差异无统计学意义(rs9616915:基因型χ2=0.452,P>0.05;等位基因χ2=0.217,P>0.05;rs13057681:基因型χ2=0.256,P>0.05;等位基因χ2=0.173,P>0.05).结论 Shank3基因rs9616915和rs13057681SNPs片段与中国汉族儿童孤独症的发病无关,孤独症的易感基因有待于进一步研究.     

TIAM1基因多态性与川崎病及其临床特点的相关性

目的 探讨TIAM1基因多态性与川崎病(KD)及其临床特点的相关性。方法 采取病例-对照研究方法,选取2012年3月至2014年9月诊断为KD的患儿188例为KD组,同期选取197例行健康体检的儿童作为对照组。利用PCR-RFLP方法测定TIAM1基因2个SNP位点rs2833188和rs2833195的多态性分布,并进行统计分析。结果 KD组SNP位点(rs2833188)的基因型(AA、AG、GG)和等位基因分布频率与正常对照组相比差异均无统计学意义(P>0.05);KD组SNP位点(rs2833195)基因型(CC、GC、GG)分布频率与对照组相比差异有统计学意义(P=0.017),且KD患儿C等位基因频率高于对照组(P=0.015)。SNP位点(rs2833188)的多态性和KD患儿结膜充血的易感性相关(P=0.011);而SNP位点(rs2833195)的多态性与KD患儿皮疹的易感性相关(P=0.021)。结论 TIAM1基因的SNP位点rs2833195的多态性与KD的易感性相关;SNP位点rs2833188和rs2833195的多态性可能与KD患儿的部分临床特点的发生相关。     

Plasma long-chain fatty acids profile and metabolic outcomes in normolipidaemic obese children after one-year nutritional intervention

Aim: To assess the association between changes in plasma long‐chain polyunsaturated fatty acids (LCPUFAs) profile and metabolic outcomes after 1‐year nutritional intervention in normolipidaemic obese children. Methods: Fifty‐seven normolipidaemic obese children, aged 8–13 years, were recruited in the study. Body mass index (BMI) z‐scores were calculated. Fasting blood samples were analysed for insulin, glucose, lipid profile and fatty acid (FA) levels at baseline and after an 1‐year nutritional‐behaviour intervention. Insulin resistance was estimated by homeostatic model assessment (HOMA). Results: Fifty‐one obese children completed the study. At the end of the intervention, the children showed decreased BMI z‐score (mean reduction 0.25; 95% confidence interval [CI], 0.18–0.31), HOMA index (1.6; 0.6–2.5), plasma‐saturated FA (1.49; 0.67–2.31 mg/dL), C20:3n‐9 (0.05; 0.02–0.07 mg/dL) and increased plasma levels of monounsaturated FA (mean increase 1.35; 0.63–2.07 mg/dL), n‐6 PUFA (1.02; 0.08–1.97 mg/dL), n‐3 PUFA (0.24; 0.07–0.40 mg/dL), C20:4n‐6 (0.37; 0.11–0.63 mg/dL), C18:3n‐3 (0.04; 0.01–0.07 mg/dL), C22:6n‐3 (0.30; 0.17–0.42 mg/dL) and the C22:6n‐3/C20:4n‐6 ratio (0.02; 0.01–0.03 mg/dL) ratio. Conclusions: Nutritional interventions may improve plasma LCPUFA profile and metabolic outcomes of normolipidaemic obese children.     

Type 2 diabetes mellitus in African-American adolescents: impaired beta-cell function in the face of severe insulin resistance

We have previously demonstrated abnormalities in insulin secretion in adolescents with type 2 diabetes mellitus (DM2) in response to the mixed meal test and to glucagon. In order to further assess beta-cell function in DM2, we measured insulin and C-peptide responses to oral glucose in adolescents with DM2 in comparison to non-diabetic obese and lean adolescents. We studied 20 patients with DM2, 25 obese adolescents with matching body mass index (BMI) (33.8 +/- 1.4 vs 34.3 +/- 1.0 kg/m2), and 12 non-obese control adolescents (BMI 22.6 +/- 0.6 kg/m2). Mean age, sex and sexual maturation did not differ between the three groups. All adolescents with DM2 had negative islet cell antibodies (ICA); five patients were on diet and 15 on insulin treatment. Fasting lipid profiles were determined in all participants. Plasma glucose and serum C-peptide and insulin levels were measured at 0, 30, 60, 90, and 120 min after an oral glucose load. The C-peptide increment (deltaCP) was calculated as peak minus fasting C-peptide. Area under the curve (AUC) was estimated using the trapezoid method. Insulin resistance was estimated using the HOMA model (HOMA-IR). The first phase of insulin secretion (PH1) was computed using a previously published formula. Serum triglyceride levels were significantly higher in the patients with DM2 compared to the non-obese controls (1.4 +/- 0.1 vs 0.9 +/- 0.1 mmol/l; p = 0.02). Plasma glucose AUC was greater in the patients with DM2 compared to the obese and non-obese control groups (1,660 +/- 130 vs 717 +/- 17 vs 647 +/- 14 mmol/l x min; p < 0.0001). ACP was lower in adolescents with DM2 than in obese and non-obese adolescents (761 +/- 132 vs 1,721 +/- 165 vs 1,225 +/- 165 pmol/l; p < 0.001). Insulin AUC was lower in the patients with DM2 compared to obese controls (888 +/- 206 vs 1,606 +/- 166 pmol/l x h; p = 0.009), but comparable to that of the non-obese controls (888 +/- 206 vs 852 +/- 222 pmol/l x h; p = 0.9). Insulin AUC was also higher in the obese than in the non-obese group (p = 0.05). PH1 was significantly higher in the obese group compared to the patients with DM2 as well as to the non-obese controls (2,614 +/- 2,47.9 vs 929.6 +/- 403.5 vs 1,946 +/- 300.6 pmol/l, respectively; p = 0.001). PH1 was also higher in the non-obese controls than in the patients with DM2 (p = 0.05). HOMA-IR was three-fold higher in the patients with DM2 than in the BMI-matched obese group, and five-fold higher than in the lean controls (14.3 +/- 1.2 vs 5.4 +/- 0.8 vs 2.9 +/- 0.4; p = 0.0002). Adolescents with DM2 have dyslipidemia, a significant cardiovascular risk factor. Decreased beta-cell function is characteristic of adolescents with DM2 in the presence of severe insulin resistance.     

The relation of vitamin D deficiency with puberty and insulin resistance in obese children and adolescents

The prevalence of obesity among children and adolescents has been rapidly increasing in recent years. Obese individuals are at risk for vitamin D deficiency. The aim of this study was to investigate the relation of vitamin D deficiency with puberty and insulin resistance in obese children and adolescents. A total of 106 children and adolescents (48 prepubertal and 58 pubertal) between 8 and 16 years of age were included in the study. Fasting blood glucose, insulin, lipid profile, calcium, phosphorus, alkaline phosphatase, parathyroid hormone, 25-hydroxyvitamin D [25(OH)D] levels, as well as blood glucose and insulin concentrations at 120 min of oral glucose tolerance test were measured. Insulin resistance was calculated using the homeostasis model assessment. Daily vitamin D intake was questioned. Serum 25(OH)D level was normal in only 3.8%, insufficient in 34.0%, and deficient in 62.2% of the subjects. There was a statistically significant rate of 25(OH)D deficiency in the pubertal group compared with that in the prepubertal group. Those subjects with 25(OH)D deficiency were found to have greater insulin resistance. Vitamin D deficiency is common among obese children and adolescents. Low vitamin D levels in obese individuals may accelerate the development of metabolic syndrome, type 2 diabetes mellitus, and cardiovascular disease by further increasing insulin resistance.     

PPAR-gamma2 Pro12Ala variant, insulin resistance and plasma long-chain polyunsaturated fatty acids in childhood obesity

Pro12Ala variant of peroxisome-proliferator-activated receptor-gamma2 (PPAR-gamma2) may be linked to insulin sensitivity. This study examined whether an association of PPAR-gamma2 Pro12Ala with insulin resistance and plasma LCPUFAs may exist in obese children. One hundred and forty Italian normolipidemic obese children (58 girls and 82 boys, mean age [SD], 10.2 [2.7] y) entered the study. Obesity was defined according to International Obesity Task Force. BMI Z-scores were calculated. Fasting blood glucose, insulin, lipids and plasma fatty acids were measured. Insulin resistance was estimated by the homeostatic model assessment (HOMA-IR). The frequency of Ala allele was 9%. Mean [SD] values of fasting insulin and HOMA-IR in Pro/Pro versus Pro12Ala groups were: 19.3 [10.6] versus 14.1 [10.4] microU/mL (p = 0.017) and 4.2 [2.3] versus 3.0 [2.3] (p = 0.022). Mean [SD] values of plasma C20:3n-9 and of C20:4n-6, C20:5n-3, C22:6n-3 and n-6/n-3 LCPUFA in phospholipds in Pro/Pro versus Pro12Ala groups were: 0.15 [0.07] versus 0.12 [0.08] % (p = 0.014), 8.9 [1.9] versus 10.2 [2.6] % (p = 0.023), 0.34 [0.15] versus 0.42 [0.11] % (p = 0.005), 2.1 [0.9] versus 2.6 [0.9] % (p = 0.032) and 4.8 [1.2] versus 4.2 [0.7] (p = 0.017). Pro12Ala may be associated with higher insulin sensitivity and higher LCPUFAs, particularly n-3, levels in plasma phosholipids of obese children.     

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.     

The prevalence of impaired fasting glucose and type 2 diabetes in a population‐based sample of overweight/obese children in the Middle East

Moadab MH, Kelishadi R, Hashemipour M, Amini M, Poursafa P. The prevalence of impaired fasting glucose and type 2 diabetes in a population‐based sample of overweight/obese children in the Middle East. Background: Type 2 diabetes mellitus (T2DM) and impaired fasting glucose (IFG) are increasing in young population who are facing an escalating trend of overweight. The aim of this study was to determine the prevalence of IFG and T2DM for the first time in a population‐based sample of Iranian obese children. Methods: This cross‐sectional, population‐based study was conducted in Isfahan, the second large city of Iran. Overall, 672 overweight and obese school students, selected from 7554 students, aged 6–19 yr, were screened for IFG and T2DM. Fasting plasma glucose (FPG) and lipid profile were measured in all participants. Oral glucose tolerance test and insulin level were measured in those children with IFG. Insulin resistance was defined as homeostasis model assessment for insulin resistance (HOMA‐IR) > 3.10. Results: Among the7554 students (48.7% boys and 51.3% girls) studied, 9.34% (n = 706) were overweight and 5.3% (n = 403) were obese. A number of 672 overweight and obese students including 302 (44.9%) boys and 370 (55.1%) girls, with a mean age of 12.8 ± 3.10 yr underwent biochemical work up. Overall, the prevalence of IFG was 4.61% (n = 31), the corresponding figure was 2% (n = 4) in the 6–10 yr age group, and 5% (n = 27) in those aged 10.1–19 yr. The prevalence of T2DM was 0.1% (n = 1; age, 18.00 yr). Impaired glucose tolerance and insulin resistance were detected in three and six participants with IFG, who consisted 0.4 and 0.8% of total obese and overweight students, respectively. Conclusions: Although the prevalence of T2DM is low in Iranian obese children, IFG is not uncommon. Preventive measures and screening of FPG should be considered for these children.     

肥胖儿童青少年腹部脂肪不同评价方法比较(英文)

Objectives To assess the clinical value of ultrasonography ( US) and bioelectrical impedance analysis (BIA) in analyzing abdominal fat contents of obese children and adolescents through comparison with MRI. A correlation with other obese related metabolic parameters was conducted. Methods Ninety 7-17-y-old obese children and adolescents (60 boys and 30 girls with mean age of 9.6 ± 2.9 y and mean BMI of 24.5 ± 4.5 kg / m2) were recruit- ed. Metabolic parameters were measured, and insulin resistance was estim...     

Metabolic correlates with obstructive sleep apnea in obese subjects

OBJECTIVE: To examine links between obstructive sleep apnea (OSA), insulin resistance, and dyslipidemia. STUDY DESIGN: Obese (body mass index [BMI] >95th percentile for age and gender) children who snored (n = 62, 46 males, age 10.89 [5-16 years] underwent polysomnography and metabolic studies. RESULTS: Respiratory disturbance index (RDI) was 9.23 (0-95), with 23 children (39%) recommended for treatment. Fasting insulin levels were 154.6 pmol/L +/- 79.8 (52-486), and fasting glucose levels were high in 7 children (11%). Fasting insulin levels correlated with sleep variables, including log transformed RDI (log(10)RDI) (P =.01), desaturation events (P =.05), arousal index (P =.01), and sleep-time with oxygen saturation in arterial blood <90% (P =.03) (adjusted r (2) = 0.21, F = 3.9, P =.005), but not with age, or BMI Z score. Log(10)RDI correlated with fasting insulin (P =.001) and BMI Z score (P =.03) (adjusted r (2) = 0.12, F = 3.9, P =.005), but not age or other metabolic variables. The correlation between log(10)RDI and fasting insulin persisted in models combining sleep and metabolic variables: log(10)RDI, adjusted r (2) = 0.75, F = 35.2, P <.001, and for fasting insulin, adjusted r (2) = 0.42, F = 6.1, and P <.001. CONCLUSIONS: The severity of OSA (log(10)RDI) correlated with fasting insulin levels, independent of BMI. Insulin levels may be further elevated as a consequence of OSA in obese children.     

Plasma long-chain fatty acids and the degree of obesity in Italian children

Aim: To examine whether the plasma levels of long-chain polyunsaturated fatty acids (LC-PUFAs) are associated with the degree of obesity in children. Methods: Sixty-seven normolipidaemic obese children, aged 8-12 y, and 67 age- and sex-matched normal-weight children were included in the study. Obesity was defined in accordance with the International Obesity Task Force. BMI z-scores were calculated. Fasting blood samples were analysed for insulin, glucose, lipid profile and fatty acid (FA) levels (expressed as % total FA). Insulin resistance was estimated by homeostatic model assessment (HOMA). Results: Compared with normal-weight children, obese children exhibited lower mean plasma total PUFA (37.8% vs 39.7%), ω-6 PUFAs (35.0% vs 36.8%) and C_{22:6 ω-3}-to-C_{18:3 ω-3} ratio (5.52 vs 7.61), and higher total monounsaturated FA (26.6% vs 25.0%), C_{18:3 ω-3} (0.28% vs 0.25%) and C_{20:5 ω-3} (0.45% vs 0.39%). In obese children, the BMI z-score was negatively related to plasma PUFA, ω-3 PUFAs, C_{22:6 ω-3}, and the C_{22:6 ω-3}-to-C_{20:6 ω-6} and C_{22:6 ω-3}-to-C_{18:3 ω-3} ratios, and positively with total saturated FA and C_{20:3 ω-9}.



Conclusion: In obese children, plasma LC-PUFA profile may be associated with the degree of obesity.     

肥胖儿童伴良性黑棘皮病与胰岛素抵抗19例分析

目的　探讨肥胖儿童伴良性黑棘皮病与胰岛素抵抗及 2型糖尿病的关系。方法2 0 0 3年 6月～ 2 0 0 3年 9月 ,在我院内分泌门诊及病房就诊的体重指数 (BMI)≥ 2 5的肥胖儿童共 76例 ,对其中伴黑棘皮病皮肤改变的 19例 ( 2 5 % )均行皮肤病理活检以明确诊断 ,同时对这些患儿行空腹血糖、空腹血胰岛素水平、空腹血糖 /胰岛素比值 (FGIR)及人体测量学参数 [腰围 /臀围比值(WHR) ,全身体脂含量 (FM)、体脂百分数 (BF % )、体重指数 (BMI) ]等的检测 ,并行葡萄糖耐量试验(OGTT试验 ) ,以探讨肥胖儿童伴良性黑棘皮病与胰岛素抵抗及 2型糖尿病的关系。结果　 19例良性黑棘皮病患儿人体测量学参数包括腰围 /臀围比值 ,全身体脂含量 (FM)、体脂百分数 (BF % )、体重指数 (BMI)及空腹血胰岛素水平明显高于正常对照组 (P <0 0 1) ,空腹血糖 /胰岛素比值 (FGIR) ( 4 2 7± 0 5 3)小于 7,存在明显的胰岛素抵抗 ,其中 1例诊断为 2型糖尿病 ,10例有糖耐量异常。结论　儿童良性黑棘皮病与肥胖、高胰岛素血症 ,胰岛素抵抗及 2型糖尿病密切相关 ,是临床胰岛素抵抗的皮肤标志