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。     

��ͬ������״̬���ֶ�ͯѪ��֬���صı仯�����ٴ�����

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。     

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     

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。     

肥胖儿童糖耐量试验结果分析

为了解肥胖儿童糖耐量低减和II型糖尿病的发生情况,检测10例肥胖儿童的空腹胰岛素,血脂常规并进行糖面量试验,结果:10例肥胖患儿中,糖耐量正常者4例,糖耐量低减者4例,II型糖尿病2例,肥胖组空腹胰岛纱和服糖后2小时血糖均显著高于对照组（P＜0．01,P＜0．001）,空腹血糖也高于正常对照组,但无统计学意义,结论：有糖尿病家族中的肥胖儿童,更容易出现胰岛素抵抗和糖耐量异常,甚至发生I 病,研究肥胖儿童和II型糖尿病的胰岛β－细胞功能和胰岛素低抗变化的相关机制,将有助于早期干预和控制儿童II型糖尿病。     

减肥对单纯性肥胖儿童糖耐量及胰岛素分泌功能的影响

目的探索单纯性肥胖儿童糖耐量减低(IGT)的干预方法。方法测定14例单纯性肥胖儿童经日服葡萄糖耐量实验(OGTT),诊断为IGT,男10例,女4例;年龄8-15岁;体质量(57.7-114.0)kg,体质量指数(BMI)(30.18±1.71)。给予中医循经推拿和行为矫正及饮食、运动调整综合减重治疗2个月。结果14例IGT肥胖儿童减肥治疗2个月后9例OGTT恢复正常,体质量下降至(49-95)kg;BMI下降至(25.30±1.35)kg;治疗后空腹胰岛素、餐后2 h胰岛素、餐后2 h血糖[(14.23 ±2.35)mIU/L、(47.20±10.26)mIU/L、(5.63±0.91)mmol/L]较治疗前[(32.54±7.13)mIU/L、(164.53±33.60)mIU/ L、(8.75±1.09)mmol/L]明显下降(P<0.05,<0.01,<0.05);空腹血糖(4.80±0.52)mmol/L和治疗前(5.36±1.59) mmol/L比较无明显差异(P>0.05)。结论减肥是干预单纯性肥胖儿童IGT、改善胰岛素抵抗及预防2型糖尿病的最好方法。     

肥胖儿童脂肪肝与胰岛素抵抗的关系

目的了解肥胖儿童非酒精性脂肪肝(NASH)的发病情况及与胰岛素抵抗的关系。方法对125例肥胖儿童行肝脏B超检查及血生化检查;对其中36例肥胖伴NASH儿童和41例无并发症的单纯肥胖儿童,以及22例对照儿童空腹行口服葡萄糖耐量和胰岛素释放试验,计算体重指数(BMI)、稳态模型胰岛素抵抗指数(HOMA蛳IR)、总体胰岛素敏感指数(WBISI)和葡萄糖、胰岛素曲线下面积之比(AUCINS/AUCBG)。结果NASH在肥胖儿童中的发生率为28.8%;NASH组BMI、HOMA蛳IR、AUCINS/AUCBG均明显高于单纯肥胖组和对照组熏WBISI明显低于单纯肥胖组和对照组;单纯肥胖组HOMA蛳IR、AUCINS/AUCBG均明显高于对照组。结论肥胖儿童中NASH发生率较高;NASH儿童存在严重的胰岛素抵抗,胰岛素抵抗可能是NASH重要发病机制之一。     

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。     

单纯性肥胖患儿胰岛素抵抗与血脂的关系

目的探讨单纯性肥胖(肥胖)患儿胰岛素抵抗与血脂的关系。方法选取肥胖患儿50例为肥胖组(男23例,女27例),同期健康儿童30例为健康对照组(男14例,女16例)。对每位对象采用同一磅秤标准,测量其身高、体质量,并计算其体质量指数(BMI)。采用儿童标准血压测定法测定2组儿童血压。采用发光免疫法、快速测血糖法分别对2组儿童的血糖、血胰岛素、血脂进行检测,并计算稳态模型胰岛素抵抗指数(HOMA-IR)、胰岛素敏感指数(HOMA-ISI)、胰岛素和葡萄糖曲线下的面积比值反映组织对胰岛素的敏感性(AUC)、肝脏组织对胰岛素的敏感性(FINS/FBG),并应用SPSS12.0软件进行统计学分析。结果与健康对照组比较,肥胖组患儿HOMA-IR、AUC、FINS/FBG均显著增高(t=3.939、6.314、3.723,Pa<0.01),空腹三酰甘油(TG)亦显著增高(t=2.573,P<0.05),高密度脂蛋白(HLD)、HOMA-ISI显著低于健康对照组(t=-2.982、-4.75,P<0.05、0.01)。多因素Pear-son相关分析显示,肥胖组TG与HOMA-IR、AUC、FINS/FBG呈显著正相关(r=0....     

The abnormalities of carbohydrate metabolism in Turner syndrome: analysis of risk factors associated with impaired glucose tolerance

An oral glucose tolerance test (OGTT) was performed in 103 patients with Turner syndrome (TS) who had normal fasting and postprandial glucose levels. The plasma glucose, insulin, C-peptide and proinsulin levels were measured every 30 min during the test. Using a homeostatic model assessment (HOMA) and a quantitative insulin sensitivity check index (QUICKI), the insulin resistance in TS patients was investigated. Diabetes mellitus and impaired glucose tolerance (IGT) were newly diagnosed in two and 18 patients respectively. There was a significant increase in mean plasma glucose, insulin, C-peptide and proinsulin reponse during an OGTT in the IGT group in contrast to the normal glucose tolerance (NGT) group ( P <0.05). There was a significant decrease in the quantitative insulin sensitivity check index (QUICKI) in the IGT group in contrast to the NGT group ( P <0.05). The fasting insulin and triglyceride levels strongly predicted the 2 h glucose level during the OGTT ( P <0.05). Conclusion:The oral glucose tolerance test is superior to the fasting and postprandial plasma glucose test for the early detection of abnormalities of carbohydrate metabolism in patients with Turner syndrome.     

Glucose tolerance status in 510 children and adolescents attending an obesity clinic in Central Italy

Brufani C, Ciampalini P, Grossi A, Fiori R, Fintini D, Tozzi A, Cappa M, Barbetti F. Glucose tolerance status in 510 children and adolescents attending an obesity clinic in Central Italy. Childhood obesity is epidemic in developed countries and is accompanied by an increase in the prevalence of type 2 diabetes (T2DM). Aims: Establish prevalence of glucose metabolism alterations in a large sample of overweight/obese children and adolescents from Central Italy. Methods: The study group included 510 overweight/obese subjects (3–18 yr). Oral glucose tolerance test (OGTT) was performed with glucose and insulin determination. Homeostatic model assessment of insulin resistance (HOMA‐IR) and insulin sensitivity index (ISI) were derived from fasting and OGTT measurements. Beta‐cell function was estimated by insulinogenic index. Fat mass was measured by dual‐energy x‐ray absorptiometry. Results: Glucose metabolism alterations were detected in 12.4% of patients. Impaired glucose tolerance (IGT) was the most frequent alteration (11.2%), with a higher prevalence in adolescents than in children (14.8 vs. 4.1%, p < 0.001); silent T2DM was identified in two adolescents (0.4%). HOMA‐IR and glucose‐stimulated insulin levels were higher in patients with IGT than individuals with normal glucose tolerance (HOMA‐IR = 4.4 ± 2.5 vs. 3.4 ± 2.3, p = 0.001). Fat mass percentage and insulinogenic index were not different between the two groups. In multivariate analysis, age, fasting glucose, and insulin resistance influenced independently plasma glucose at 120 min of OGTT. Individuals with combined impaired fasting glucose/IGT (IFG/IGT) and T2DM were older and had reduced plasma insulin values at OGTT when compared to patients with simple IGT. Conclusions: Glucose metabolism alterations are frequently found among children and adolescents with overweight/obesity from Central Italy. Age, fasting glucose, and insulin resistance are main predictors of IGT. We suggest the use of OGTT as a screening tool in obese European adolescents.     

肥胖伴黑色棘皮病儿童胰岛分泌功能的临床研究

目的　研究肥胖伴黑棘皮病儿童胰岛素分泌功能的改变 ,探讨其临床意义。方法　对35例肥胖伴黑色棘皮病患儿、38例单纯肥胖患儿及 39例正常儿童进行胰岛 β细胞功能指标的测定。结果　肥胖伴黑色棘皮病组空腹胰岛素、C肽、胰岛素原、真胰岛素、胰岛素原与胰岛素、C肽比值、胰岛素抵抗指数和胰岛 β细胞分泌指数 (中位数及范围 )分别为 18 5 (5 0～ 6 0 5 )pmol/L、3 9(1 3～14 0 ) μg/L、2 8 84 (9 9～ 6 4 2 )pmol/L、32 96 (6 2～ 6 6 0 )pmol/L、1 2 (0 4～ 8 9)、6 9(2 5～ 36 6 )、5 0(0 8～ 14 1)和 30 3 3(5 2 2～ 116 3 8) ,均显著高于单纯肥胖组和正常组 (P <0 0 0 1)。结论　肥胖伴黑色棘皮病已经存在严重的胰岛 β细胞分泌亢进和胰岛素抵抗 ,是儿童患 2型糖尿病的高危 信号     

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.     

Alterations of glucoregulation in childhood obesity--association with insulin resistance and hyperinsulinemia

AIM: To study the prevalence of alterations of glucoregulation in childhood obesity. PARTICIPANTS: 250 obese children. Oral glucose tolerance test was performed, serum glucose and insulin were determined, and HOMA-IR was calculated. RESULTS: Impaired fasting glucose (IFG) was found in 1.2% according to World Health Organisation criteria and 4.4% according to the criteria of the International Diabetes Federation. Impaired glucose tolerance (IGT) was found in 13.6%, type 2 diabetes mellitus (DM2) in 2.4%. Frequency of fasting glucose (FG) above 7.0 mmol/l was 1.2%. Basal hyperinsulinemia was increased in 70%, reactive hyperinsulinemia in 88%, frequency of elevated HOMA-IR was 78%. 120' insulin was increased in all cases with abnormal FG, IGT and DM2, HOMA-IR was elevated in 79% of patients with IGT and all patients with abnormal FG and DM2. Significant positive correlations were demonstrated between body mass index and insulin levels. CONCLUSION: Our data show that hyperinsulinemia can successfully compensate for insulin resistance in the majority of the obese children. Since IFG is less frequent than IGT there is a need for performing OGTT to demonstrate abnormality of glucoregulation in 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.     

Glucose metabolism disorder in obese children assessed by continuous glucose monitoring system

Background  Continuous glucose monitoring system (CGMS) can measure glucose levels at 5-minute intervals over a few days, and may be used to detect hypoglycemia, guide insulin therapy, and control glucose levels. This study was undertaken to assess the glucose metabolism disorder by CGMS in obese children. Methods  Eighty-four obese children were studied. Interstitial fluid (ISF) glucose levels were measured by CGMS for 24 hours covering the time for oral glucose tolerance test (OGTT). Impaired glucose tolerance (IGT), impaired fasting glucose (IFG), type 2 diabetic mellitus (T2DM) and hypoglycemia were assessed by CGMS. Results  Five children failed to complete CGMS test. The glucose levels in ISF measured by CGMS were highly correlated with those in capillary samples (r=0.775, P<0.001). However, the correlation between ISF and capillary glucose levels was lower during the first hour than that in the later time period (r=0.722 vs r=0.830), and the ISF glucose levels in 69.62% of children were higher than baseline levels in the initial 1–3 hours. In 79 obese children who finished the CGMS, 2 children had IFG, 2 had IGT, 3 had IFG + IGT, and 2 had T2DM. Nocturnal hypoglycemia was noted during the overnight fasting in 11 children (13.92%). Conclusions  Our data suggest that glucose metabolism disorder including hyperglycemia and hypoglycemia is very common in obese children. Further studies are required to improve the precision of the CGMS in children.     

Relationship between plasma leptin, insulin and tumor necrosis factor alpha in obese children

OBJECTIVES: 1. To evaluate the relationship between plasma leptin and TNFalpha concentrations in obese children and to assess the differences between hyperinsulinemic and normoinsulinemic groups. 2. To evaluate the relationship between plasma leptin and insulin levels in obese children. 3. To investigate the TNFalpha G308A mutation in obese children. METHODS: Body mass index (BMI), fasting plasma glucose and insulin levels, oral glucose tolerance test results, homeostasis model assessment of insulin resistance (HOMA-IR) results, and plasma leptin and TNFalpha concentrations were evaluated in obese children (n = 45) and age- and gender-matched, lean healthy controls (n = 40). RESULTS: In obese children the fasting insulin, HOMA-IR results, plasma leptin and TNFalpha concentrations were significantly higher than in controls (p <0.05). Furthermore, obese females showed higher plasma leptin and insulin resistance compared to obese males. While plasma leptin, TNFalpha levels and HOMA-IR results were similar in the prepubertal and pubertal groups, insulin levels were significantly higher in the pubertal group. Plasma leptin and TNFalpha concentrations were similar in hyperinsulinemic and normoinsulinemic obese children. In control children, plasma leptin concentrations showed a positive correlation with BMI, age, fasting insulin and HOMA-IR results. In obese children, plasma leptin levels did not correlate with BMI, fasting insulin or TNFalpha. CONCLUSION: Plasma leptin concentrations did not show any correlation with TNFalpha levels in obese children. Furthermore, plasma leptin and TNFalpha concentrations were similar in hyperinsulinemic and normoinsulinemic obese children.