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     

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。     

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。     

单纯性肥胖儿童血浆内脂素水平与相关因素分析

目的 探讨单纯性肥胖儿童血浆内脂素水平与相关因素的关系.方法 2006年2月至2007年2月在天津医科大学总医院儿科内分泌门诊采用酶联免疫法测定50例单纯性肥胖儿童和30名正常对照的血浆内脂素.并分析血浆内脂素与收缩压、舒张压、体质量指数、体脂百分比、腰围、腰臀比及空腹血糖、空腹胰岛素水平、胰岛素抵抗指数、胰岛素敏感性指数及血脂的相关关系.结果 (1)肥胖组血浆内脂素质量浓度为(32.26±6.83)μg/L,对照组为(25.69±8.05)μg/L,肥胖组明显高于对照组(P<0.01).(2)内脂素与年龄、性别无相关关系;与体质量指数、体脂百分比、空腹血糖和胰岛素抵抗指数呈显著的正相关(相关系数r分别为0.333、0.301、0.486、0.290,P<0.01);与收缩压、舒张压、腰围、腰臀比、空腹胰岛素水平呈正相关(相关系数r分别为0.280、0.278、0.242、0.273、0.221.P<0.05);与胰岛素敏感性指数、高密度脂蛋白呈负相关(相关系数r分别为-0.269、-0.222.P<0.05);与总胆固醇、三酰甘油(甘油三酯)、低密度脂蛋白无相关关系.(3)多元逐步回归分析表明空腹血糖为影响内脂素最为显著的因素,标准化偏回归系数为0.486(P<0.01),R2=0.236.结论 血浆内脂素水平与肥胖程度、脂肪分布、糖、脂代谢密切相关.初步提示内脂素可能与儿童肥胖的发生发展密切相关.     

高敏C反应蛋白水平与肥胖及糖代谢异常儿童相关因素的研究

目的 了解高敏C反应蛋白（hs-CRP）与肥胖及糖代谢异常儿童的体量指标及血清参数相关性;探讨hs-CRP与儿童肥胖患者及糖尿病或糖代谢异常的关系。方法 选择肥胖儿童70例作为研究对象,并选择正常儿童30例作为对照组（组1）,根据OGTF试验将肥胖儿童分为不伴糖代谢异常组54例（组2）和糖代谢异常组16例（组3）,测定体量指标及相关参数。结果 肥胖儿童hs-CRP水平2．44（0．01～14．6）mg／L,明显高于对照组[0．1（0．01-2．1）mg／L]。血糖和血脂于正常范围时,肥胖儿童的hs-CRP水平为2．4（0．01-9．0）mg／L,胰岛素抵抗指数（IRI）明显升高。糖脂代谢异常时,hs-CRP水平为2．6（0．1-14．6）mg／L。Pearson相关分析显示,血清hs-CRP水平与BMI、腰围、臀围、腰臀比呈正相关,其中与BMI的相关性最强,多元线性回归分析示,BMI是惟一与hs-CRP相关的指标。结论 肥胖儿童存在低度炎症状态和胰岛素抵抗。hs-CRP与BMI独立相关。hs-CRP和胰岛素抵抗指数的异常升高早于血糖和血脂,hs-CRP增高对糖脂代谢的异常有较好的预测能力。     

非酒精性脂肪性肝病肥胖儿童人体成分及其影响因素分析

目的 分析肥胖儿童非酒精性脂肪性肝病（NAFLD）人体成分及其影响因素，为临床防治提供依据。方法纳入2019年1月至2021年7月首都医科大学附属北京儿童医院就诊236例肥胖儿童，依据诊断标准分组：NAFLD组135例、非NAFLD组101例。采用人体成分分析仪检测人体成分，并收集患儿一般资料，完善血生化、糖化血红蛋白、空腹胰岛素、空腹C肽、腹部彩超等检查，分析各指标特点。结果 236例肥胖患儿中男148例、女88例，年龄4～17岁，平均年龄为（9.78±2.39）岁。236例中体脂肪升高232例、体脂百分比升高235例，蛋白质升高22例、无机盐升高23例、肌肉量升高32例。两组指标体重指数、体脂肪、蛋白质、无机盐、体脂百分比、内脏脂肪面积、无脂肪质量指数（SMMI）、肌肉质量指数（FFMI）、基础代谢量比较，NAFLD组高于非NAFLD组，差异有统计学意义（P相似文献   

肥胖伴黑棘皮病儿童代谢综合征的高危因素

目的 探讨肥胖伴黑棘皮病儿童代谢综合征(MS)的高危因素.方法 2006年11月-2007年9月在本院儿科就诊25例肥胖伴黑棘皮病儿童(病例组).男15例,女10例;年龄8.4～16.0岁,平均10.6岁;体质量(72.11±17.66)kg;身高(155±14)cm.32例身高别体质量正常的健康儿童为健康对照组.男18例,女14例;年龄7.6～15.8岁,平均9.8岁.比较二组儿童体质量指数(BMI)、胆固醇(12HO)、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-C)、血压、空腹和葡萄糖耐量试验(OGTT)2 h血糖、胰岛素和稳态模型评估法胰岛素抵抗指数(HOMA-IR)的差异,并对所有儿童进行肝脏超声波检查.采用SPSS 12.0软件进行统计学分析.结果 病例组儿童BMI、TG、LDL-C、收缩压和舒张压均显著高于健康对照组(Pa<0.01);空腹和OGTT 2h血糖、OGTT 2h胰岛素和HOMA-IR均显著高于健康对照组(Pa<0.01);BMI与收缩压、舒张压、CHO、TG、LDL-C、空腹血糖(FBG)、空腹胰岛素(FINS)以及HOMA-IR均无相关性(Pa>0.05).病例组患儿中超声诊断脂肪肝发生率为84%,健康对照组儿童肝脏B超检查均未见异常.结论 肥胖伴黑棘皮病儿童BMI增加、胰岛素抵抗、血脂紊乱和血压增高是MS的危险因素,密切随访监测此类患儿有助于早期发现MS.积极治疗肥胖症,阻断儿童血糖、血脂代谢紊乱的发生,有助于减少儿童2型糖尿病和心血管疾病的危险性.     

血清microRNA-122与肥胖儿童胰岛素抵抗的关系

目的 研究肥胖儿童血清microRNA-122（miR-122）与胰岛素抵抗的关系。方法 选取47例7~14岁重度肥胖儿童为肥胖组,另选取与肥胖组性别及年龄匹配的正常体重健康儿童45例作为健康对照组,分别检测并记录两组儿童的身高、体重、腰围、臀围、空腹血糖（FBG）、空腹胰岛素（FINS）、甘油三酯（TG）、总胆固醇（TC）、游离脂肪酸（FFA）、白介素-6（IL-6）、miR-122水平,计算体重指数（BMI）、腰臀比（WHR）、胰岛素抵抗指数（HOMA-IR）,并进行统计分析。结果 与健康对照组相比,肥胖组儿童身高、体重、BMI、WHR及FINS、HOMA-IR、TG、FFA、IL-6、miR-122水平均升高（P < 0.05）;肥胖组miR-122水平与FINS、HOMA-IR、IL-6水平呈正相关（分别r=0.408、0.442、0.464,P < 0.05）;miR-122的变化与IL-6有线性回归关系,且呈正相关（b'=0.318,P < 0.05）。结论 肥胖儿童血清miR-122可能与胰岛素抵抗相关,具体机制尚需进一步研究。     

非酒精性脂肪肝病儿童、青少年的肝内脂肪定量评价

目的：量化评估非酒精性脂肪肝病(NAFLD)儿童、青少年肝内脂肪的临床意义。方法：对93例肥胖儿童、青少年进行形体学参数、肝功能、血脂、血糖及胰岛素释放试验和肝脏B超等检查,采用氢质子磁共振波谱定量测定肝内脂肪（IHF）含量,并按传统诊断标准将其分为单纯性肥胖组（31例）、非酒精性脂肪肝病-1组（NAFLD-1,33例）（B超示脂肪肝,但不伴有肝损）和NAFLD-2组（B超示脂肪肝,且伴有肝损,29例）。20例健康儿童、青少年作为正常对照组。观察IHF含量在组间的变化情况,分析IHF含量与各临床生化指标的相关关系以及探寻IHF量化改变的影响因素。结果：正常对照组、单纯性肥胖组、NAFLD-1组和NAFLD-2组IHF含量分别为0.80%（0.4%～1.0%）、2.9%（1.7%～4.3%）、14.0%（7.2%～17.5%）、18.8%（14.0%~29.1%）,组间两两比较差异均有统计学意义（P<0.05）。单因素相关分析表明IHF含量与腰围、臀围、腰臀比、体重指数、收缩压、舒张压、丙氨酸氨基转移酶、门冬氨酸氨基转移酶、γ-谷氨酰转肽酶、空腹甘油三酯、低密度脂蛋白、口服葡萄糖耐量试验（OGTT）2 h血糖、空腹胰岛素、2 h胰岛素和胰岛素抵抗指数呈显著正相关,与高密度脂蛋白呈显著负相关。进一步的多元线性回归分析发现增加的腰围、降低的高密度脂蛋白水平和增高的OGTT 2 h血糖是IHF含量升高的独立危险因素。结论：IHF量化改变非常敏感,早期已增高于单纯性肥胖儿童、青少年,并随NAFLD的发生、发展进程而显著升高。量化的IHF与诸多临床生化指标相关,其中腰围、高密度脂蛋白和OGTT 2 h血糖是IHF含量的独立影响因素。     

肥胖儿童糖脂代谢与膳食摄入

目的 分析肥胖儿童糖脂代谢异常情况及其膳食结构.方法 入选门诊肥胖患儿57例,男41例、女16例,年龄7～16岁.测定其人体成分、血压、血脂、血糖和胰岛素,其中21例进行连续3d的膳食调查.结果 57例患儿中共有34例(59.6%)血糖和(或)血脂代谢异常.体质指数(BMI)与空腹胰岛素(FINS)、餐后2h胰岛素(2hINS)、胰岛素抵抗指数(IRI)、腰臀比、收缩压(SBP)和舒张压(DBP)呈正相关.糖脂代谢异常组患儿的SBP、血三酰甘油(TG)和低密度脂蛋白胆固醇(LDL-C)明显高于糖脂代谢正常组(P<0.05);糖脂代谢异常的患儿膳食中饱和脂肪酸(SFA)和单不饱和脂肪酸(MUFA)摄人明显高于代谢正常的患儿(P均<0.05),而多不饱和脂肪酸(PUFA)的摄人则低于代谢正常的患儿(P<0.05).结论 肥胖儿童普遍存在糖脂代谢紊乱、脂肪酸摄入不合理.     

Characterisation of morbidity in a UK, hospital based, obesity clinic.

AIM: To identify clinical features which predict those most at risk of co-morbidities within an obesity clinic. METHODS: Children attending an obesity clinic had fasting glucose, insulin, and lipids measured prior to a standard oral glucose tolerance test (OGTT). History and examination established birth weight, family history of type 2 diabetes/obesity, pubertal status, and presence of acanthosis nigricans. Central and total fat mass was estimated by bio-impedance. RESULTS: Of the 126 children evaluated, 10.3% (n = 13) had impaired glucose tolerance (IGT); the majority (n = 11) of these would not have been identified on fasting glucose alone. Those with IGT were more likely to have a parental history of type 2 diabetes (relative risk 3.5). IGT was not associated with acanthosis nigricans. Twenty five per cent (n = 19) of those evaluated (n = 75) had evidence of the "metabolic syndrome" (MS). HDL cholesterol and triglyceride levels were related to insulin sensitivity (HOMA-R); HDL cholesterol was also related to birth weight SDS. We observed a trend for those with MS to have a lower birth weight SDS. The severity of obesity did not influence the likelihood of IGT or MS. CONCLUSIONS: Significant numbers of obese children have associated co-morbidities. Analysis of fasting blood glucose samples alone is not satisfactory to adequately evaluate glucose homoeostasis. The overall level of obesity does not predict co-morbidities. Special attention should be given to those with parental diabetes and a history of low birth weight who are more likely to have IGT and abnormal lipid profiles respectively.     

Type 2 diabetes,polycystic ovary syndrome and the insulin resistance syndrome in adolescents: Are they one big iceberg?

Obesity in children may cause overt clinical disease in childhood. The complex endocrine and metabolic changes of obesity and insulin resistance in adolescents result in hyperinsulinemia, dyslipidemia, hypertension, steatohepatitis, glucose intolerance, type 2 diabetes, acanthosis nigricans and ovarian hyperandrogenemia, commonly known as polycystic ovarian syndrome (PCOS). Type 2 diabetes and PCOS in adolescents are new endocrine diseases in this age group that require unique approaches to diagnosis and treatment. The direct correlation between duration of disease and control of the disease, and subsequent long term complications of these two diseases, predict serious morbidity in young adult life for the affected adolescents. Pediatricians have an important role in the prevention, diagnosis and treatment of obesity, insulin resistance syndrome, type 2 diabetes and PCOS.     

Insulin resistance in obese boys with acanthosis nigricans.

Insulin resistance was investigated in three obese boys with acanthosis nigricans and their results were compared to those obtained in non-acanthotic obese patients. Blood glucose immune reactive serum insulin and C-peptide during oral glucose tolerance test and 125I-insulin binding investigated. Obese patients with acanthosis nigricans were more insulin resistant than simple obese controls. Insulin binding studies performed in two acanthotic patients suggested that one of them had insulin resistance type A, and the second patient had insulin resistance type B. According to the results acanthosis nigricans can serve as a marker for severe insulin resistance in obesity.     

Obesity, acanthosis nigricans, insulin resistance, and hyperandrogenemia: pediatric perspective and natural history

We studied the syndrome of acanthosis nigricans, obesity, insulin resistance, and hyperandrogenemia in 22 patients. Although isolated case reports in adolescents have appeared, this syndrome has not received full recognition as a pediatric entity. Our patients (17 girls, five boys) had a mean weight 5.7 SD above the mean for age, although mean height was only 0.5 SD above the mean for age. All patients had acanthosis nigricans. Their insulin resistance was significantly greater than that in a control group with comparable obesity. Fasting insulin concentration was 5.25 microU/ml in lean controls, 19.6 microU/ml in obese controls, and 49.8 microU/ml in study patients (P less than 0.002). Mean glucose disappearance rate during an insulin tolerance test was 6.7%/min in lean controls, 5.19%/min in obese controls, and 2.35%/min in study patients (P less than 0.02). After menarche, mean plasma testosterone concentration was 106 ng/dl, compared with less than 50 ng/dl in all lean and obese control patients. Data derived from our series of patients lead us to conclude that (1) this is a genetic syndrome, although the exact mode of inheritance is unclear; (2) the natural history of the syndrome invariably begins with the onset of obesity, followed by acanthosis nigricans that worsens with progressive weight gain; (3) acanthosis nigricans is thus a marker for hyperinsulinemia, which occurs before hyperandrogenemia; (4) hyperandrogenemia occurs only after menarche. Identification of this syndrome should permit monitoring for the development of hyperandrogenemia during puberty and determination of other affected family members.     

Body fat distribution in childhood obesity: association with metabolic risk factors

OBJECTIVES: To evaluate the clinical significance of body fat distribution in childhood obesity, we investigated the associations of subcutaneous and intraabdominal (preperitoneal and visceral) fat, estimated by ultrasonography, with metabolic risk factors. SUBJECTS: Fifty-one obese (age 11.5+/- 2.6 years) and 33 non-obese (age 12.2+/- 2.7 years) children. STUDY DESIGN: Case control study. METHODS: Ultrasonographic measurements of fat thickness [maximum and minimum preperitoneal fat thicknesses (Pmax, Pmin), maximum and minimum subcutaneous fat thicknesses (Smax, Smin), visceral fat thickness (V), triceps (Tr) and subscapular (Ss) skin fold thicknesses] were documented. Blood pressures, lipid profiles, fasting insulin levels, glucose/insulin ratio and HOMA IR (homeostasis model assessment for insulin resistance) were evaluated in both groups and these parameters were correlated with body fat distribution. RESULTS: In the obese group, fasting insulin level was correlated to Smin, Smax, and Pmin. HOMA, accordingly, was also correlated to Smin, Smax, and Pmin. Fasting insulin level and HOMA showed no correlation with either Pmax or visceral fat thickness. ANALYSIS: Abdominal subcutaneous fat thickness measurements were the best predictors of hyperinsulinemia (R2: 0.32). CONCLUSION: We did not observe a significant correlation between blood pressure, lipid parameters and body fat distribution in obese group. Abdominal subcutaneous fat thickness might be a better predictor of the risk for hyperinsulinemia in childhood obesity.     

Relationship of body fat distribution to metabolic complications in obese prepubertal girls

The purpose of this study is to assess the relative effects of body fat distribution and obesity "per se" on serum glucose, insulin, and insulin resistance. Seventeen obese and nine nonobese control prepubertal girls were studied. Biceps, triceps, subscapular, and suprailiac skinfold thickness were measured. Percentage of body fat (% BF) and total body fat (TBF) were calculated. Body fat distribution was assessed by analyzing the central (suprailiac, subscapular)/peripheral (biceps, triceps) ratios. Oral glucose tolerance test was performed. Serum glucose and insulin were measured and insulinogenic index (insulin/glucose) was calculated. Body fat anthropometric data and body fat distribution indexes were significantly higher (p less than 0.001) in the obese group. The obese population presented significantly elevated values of glucose, insulin, and insulinogenic indexes (p less than 0.01-p less than 0.001). In the obese group, insulin showed significant positive correlations (p less than 0.05-p less than 0.001) with biceps, subscapular, and suprailiac skinfolds, % BF and TBF, whereas the insulinogenic index had positive correlations with suprailiac skinfold and TBF (p less than 0.05). Obese girls showed positive correlations between the body fat distribution indexes and insulin or insulinogenic indexes (p less than 0.05-p less than 0.001). In prepubertal girls obesity is of the centripetal (central) type. This pattern has an important role in determining the alterations in the glucose-insulin homeostasis that characterize the childhood nutritional obesity.     

Characterisation of morbidity in a UK, hospital based, obesity clinic

Aim

To identify clinical features which predict those most at risk of co‐morbidities within an obesity clinic.

Methods

Children attending an obesity clinic had fasting glucose, insulin, and lipids measured prior to a standard oral glucose tolerance test (OGTT). History and examination established birth weight, family history of type 2 diabetes/obesity, pubertal status, and presence of acanthosis nigricans. Central and total fat mass was estimated by bio‐impedance.

Results

Of the 126 children evaluated, 10.3% (n = 13) had impaired glucose tolerance (IGT); the majority (n = 11) of these would not have been identified on fasting glucose alone. Those with IGT were more likely to have a parental history of type 2 diabetes (relative risk 3.5). IGT was not associated with acanthosis nigricans. Twenty five per cent (n = 19) of those evaluated (n = 75) had evidence of the “metabolic syndrome” (MS). HDL cholesterol and triglyceride levels were related to insulin sensitivity (HOMA‐R); HDL cholesterol was also related to birth weight SDS. We observed a trend for those with MS to have a lower birth weight SDS. The severity of obesity did not influence the likelihood of IGT or MS.

Conclusions

Significant numbers of obese children have associated co‐morbidities. Analysis of fasting blood glucose samples alone is not satisfactory to adequately evaluate glucose homoeostasis. The overall level of obesity does not predict co‐morbidities. Special attention should be given to those with parental diabetes and a history of low birth weight who are more likely to have IGT and abnormal lipid profiles respectively.     

Presence of metabolic cardiovascular syndrome in obese children

The aim of the present study was to investigate the aggregation of cardiovascular risk factors (hyperinsulinaemia, impaired glucose tolerance, dyslipidaemia, and hypertension) in 180 (77 female, 103 male) obese and 239 control children. Blood glucose, serum insulin and lipid levels were determined from blood samples taken after an overnight fast. Oral glucose tolerance tests were performed and blood glucose concentrations were monitored. The body mass index, body fat (on the basis of skinfold measurements), lean body mass and waist/hip ratio were calculated and blood pressure was measured five times in all subjects. It was shown that only 14.4% of obese children were free from any risk factors, in contrast to 79.1% of the control children. Four risk factors (metabolic cardiovascular syndrome) were found in 8.9% of the obese children (8.7% in males and 9.l % in females) while none could be detected in controls. Considerable differences were also detected in the prevalence of one, two or three risk factors between control and obese children. Patients with the metabolic cardiovascular syndrome could not be characterized by any of the investigated anthropometric characteristics, but the duration of obesity was significantly longer in these children. Conclusion Potential risk factors for cardiovascular diseases already tend to cluster in childhood and they are strongly associated with obesity. Our observations suggest that the development of the metabolic cardiovascular syndrome has its origin in childhood. Received: 15 September 1998 / Accepted: 20 July 1999     

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