北京市超重肥胖儿童青少年中黑棘皮症检出率及与胰岛素抵抗的关系

目的 分析超重、肥胖儿童青少年黑棘皮症(AN)与胰岛素抵抗的关系,为诊断胰岛素抵抗提供临床线索.方法 以2004年北京市儿童青少年代谢综合征调研中筛查出的1 877例6～18岁超重和肥胖儿童青少年作为研究对象.测量体重指数、腰围,并检测空腹血糖、胰岛素和血脂水平,采用稳态模式评估(HOMA-IR)法,评价个体胰岛素抵抗状况.结果 超重、肥胖儿童中黑棘皮症检出率分别为12.7%和26.3%;合并AN者的腰围、胰岛素、甘酰甘油(甘油三酯)、血压均分别显著高于单纯超重、肥胖者,肥胖合并AN者的高密度脂蛋白-胆固醇水平显著低于单纯肥胖者;超重、肥胖组中AN阳性者的HOMA-IR指数几何均值(P25～P75)分别为2.81(2.13～4.12)mU/L和3.69(2.53～5.34)mU/L,分别显著高于两组AN阴性者[2.03(1.45～3.01)mU/L;2.45(1.72～3.61)mU/L](P＜0.001).结论 超过1/4的肥胖儿童罹患黑棘皮症;具有黑棘皮症表型特征的超重、肥胖儿童更容易出现代谢异常指标的改变,以及胰岛素抵抗程度的加重;黑棘皮症可以作为筛查胰岛素抵抗患儿的临床表型特征.     

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     

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。     

儿童2型糖尿病流行病学与发病机制的研究进展

儿童 2型糖尿病 (DM2 )的发病呈上升趋势 ,其发病有遗传和种族倾向 ,肥胖、胎儿宫内营养不良等环境因素与NIDDM的发病密切相关。胰岛素抵抗和胰岛素分泌不足是儿童DM2 两个主要发病机制。大量证据表明 ,肥胖是引发胰岛素抵抗的主要因素 ,脂肪细胞分泌的游离脂肪酸、瘦素、肿瘤坏死因子、脂联素、抵抗素等脂肪细胞因子与胰岛素抵抗的发生密切相关。而胰岛 β细胞功能缺陷亦是遗传和环境因素共同作用的结果。该文对近年来国内外儿童DM2 的流行病学、发病机制的研究进行综述。     

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。     

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。     

膳食纤维对儿童肥胖治疗作用的临床观察

目的　为更好地治疗儿童肥胖而开展膳食纤维减肥作用研究。方法　将 2 5 8例学龄期肥胖儿童随机分为治疗组 (n =12 9)和对照组 (n =12 9) ,两组患儿均在家中随意进餐 ,不限制饮食品种和数量。治疗组每人每天通过食品补充膳食纤维 12～ 18g。结果　治疗 10d后治疗组患儿进食量及摄入的总热量显著减少 (P <0 0 0 1) ,饥饿感显著减轻 ,粪便排泄增加。治疗组尿D -木糖排出量 (XEQ)治疗前为 (45 9 6± 2 0 4 1)mg/ 2h ,XEQ与肥胖程度高度相关 (r =0 5 17,P <0 0 1)。治疗 10d后XEQ显著下降至 (2 48 8± 75 4)mg/ 2h(t =4 2 5 8,P <0 0 0 1)。食用膳食纤维 2个月后患儿的空腹胰岛素、甘油三酯、胆固醇由 (2 0 3± 14 5 ) μIU/L、(1 6 5± 0 6 8)mmol/L、(6 0 3± 1 0 6 )mmol/L显著下降为 (7 6± 3 8) μIU/L、(0 74± 0 36 )mmol/L、(4 2 9± 0 5 3)mmol/L(P <0 0 0 1)。治疗前后血红蛋白及血清铜锌浓度无显著差异 (P >0 10 )。治疗半年后治疗组身高增长与对照组无显著差异 (P >0 10 ) ,但体重、腰围、臀围、腰围 /臀围、腰围 /身高和BMI显著减少 (P <0 0 0 1)。体重指数下降程度与纤维素食品食用量高度相关 (r =0 5 6 9,P <0 0 0 1) ,即补充膳食纤维数量较多者体重指数下降较多。结论　 (     

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     

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。     

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.     

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.     

儿童良性黑棘皮病与代谢异常

目的：观察儿童良性黑棘皮病与人体测量指标参数及代谢指标的关系,探讨儿童良性黑棘皮病与代谢性疾病的关系。方法：回顾性分析2007年2月至 2011年10月于我院诊治的29例良性黑棘皮病患儿的临床资料,以同年龄同性别同民族相匹配的32例正常儿童为对照组。比较两组儿童人体肥胖指标（体重指数、腰臀围比、体脂含量及体脂百分比）及代谢指标（血糖、胰岛素水平、血脂系列）等的不同。结果：29例良性黑棘皮病患儿体重指数、体脂含量、体脂百分数、腰臀围比、空腹血糖及胰岛素水平、甘油三酯均高于对照组（P<0.05）,而高密度脂蛋白低于对照组（P<0.05）。29例良性黑棘皮病患儿中,16例存在糖耐量异常,3例确诊为糖尿病（1例1型,2例2型）。结论：儿童良性黑棘皮病与肥胖、胰岛素抵抗及血脂异常密切相关。     

HUMAN PROINSULIN IN INSULIN-TREATED JUVENILE DIABETICS

Abstract. Human proinsulin was determined in a group of 73 diabetics, aged 5–20 years, with onset of diabetes at the age of 1–16 years and a duration of diabetes of 2–17 years. At the time of the investigation, the patients were receiving conventional 5 times crystallized insulin and all had detectable insulin binding IgC. Because of the binding of human proinsulin to insulin antibodies the serum was extracted with acid ethanol. Proinsulin was then determined in fasting serum after removal of human C-peptide which would have interfered with the proinsulin radioimmunoassay. The detection limit in normal serum not containing antibodies was 0.01 pmol/ml. The detection limit in sera that had to be extracted was approximately 0.05 pmol/ml. 31 of the patients (42 %) had detectable serum proinsulin, ranging from 0.055 to 2.00 pmol/ml. In the same group of patients, 19 (26%) had detectable C-peptide. There was a strong correlation between the concentration of human proinsulin and C-peptide ( P < 0.001). 38 normal fasting sera contained from 0 to 0.033 pmol/ml, mean ±S.D.: 0.009 ± 0.008 pmol/ml. The human proinsulin constituted from 0.1 to 92% of the total immunoreactive insulin (IRI) in the 31 patients with detectable proinsulin (mean: 8.5%). Thus it appears that proinsulin was secreted in 42% of 73 insulin treated juvenile diabetics who had had diabetes for 3–14 years, whereas C-peptide was found in 26% of the patients. The insulin antibodies bind a portion of the secreted proinsulin, prolonging its half-life and increasing its serum concentration. Hence, the levels of proinsulin in patients having insulin antibodies are not comparable to those in persons without antibodies.     

The somatotropic axis in short children born small for gestational age: relation to insulin resistance.

To determine whether hyperinsulinemia and reduced insulin sensitivity in individuals born small for gestational age (SGA) could be related to persisting abnormalities of the GH/IGF-I axis, we assessed overnight GH secretory profiles and measured fasting glucose, insulin, intact and 32,33 split proinsulin, and IGF-I levels in 16 short SGA children (age range 2.3-8.0 y) and in controls. Insulin sensitivity was calculated using the homeostasis model. Compared with short normal-birthweight controls (n = 7, age range 2.3-5.0 y), short SGA children had higher fasting insulin levels (means: 26.8 vs 20.6 pmol/L, p = 0.02), lower insulin sensitivity [means: 204 vs 284 %homeostasis model assessment (HOMA), p = 0.01], and higher beta cell function (112 vs 89 %HOMA, p = 0.04). SGA children also had lower levels of IGFBP-1 (87.0 vs 133.8, p = 0.04), but similar IGF-I levels (IGF-I SDS: -1.1 vs -1.7, p = 0.4). Compared with normal-height controls (n = 15, age range 5.6-12.1 y), SGA children had higher overnight GH secretion (GH maximum: 55.9 vs 39.6 mU/L, p = 0.01; mean: 13.1 vs 8.9, p = 0.004; minimum: 1.2 vs 0.6, p = 0.02). Interestingly, among SGA children, fasting insulin levels and insulin sensitivity were significantly related to overnight GH secretion (insulin sensitivity vs maximum GH: r = -0.68, p = 0.01; vs GH pulse amplitude r = -0.71, p = 0.007). The only hormone level significantly related to current height velocity was C-peptide (r = 0.75, p = 0.008). In conclusion, elevated fasting insulin levels and reduced insulin sensitivity in short SGA children was related to elevated levels of overnight GH secretion. We hypothesize that resistance to the somatotropic actions of GH and IGF-I in short SGA children may contribute directly to reduced insulin sensitivity.     

No evidence for a major beta-cell dysfunction in young adults born with intra-uterine growth retardation

The association between low birth weight and the later development of type 2 diabetes is well established. It has been hypothesized that in utero undernutrition may affect pancreatic beta-cell development, leading to an impaired beta-cell function in adulthood. We have previously demonstrated that intrauterine growth retardation (IUGR) is associated with insulin-resistance early in adulthood. The aim of this study was to test whether IUGR would affect beta-cell function in young adults. Twelve 25-yr-old insulin-resistant subjects with IUGR were matched for age gender and body mass index (BMI) to 13 controls. All of them had normal glucose tolerance. Mean fasting plasma glucose did not significantly differ between the group with IUGR and the control group (97 +/- 7 vs. 98 +/- 4 mg/dL; p = 0.83). Blood glucose was maintained at 124.8 +/- 6.5 vs. 126.2 +/- 7.5 mg/dL above the basal glycemia in the IUGR and control groups (p = 0.64) throughout the hyperglycemic clamp. Serum insulin concentrations did not significantly differ between the group with IUGR and the control group either during the first (0-10 min) phase (311 +/- 252 vs. 248 +/- 184 pmol/L, p = 0.85) or during the second (80-100 min) phase (575 +/- 284 vs. 559 +/- 413 pmol/L, p = 0.72). C-peptide concentrations were similar in both groups during the two phases (2.35 +/- 1.44 vs. 2.59 +/- 1.10 nmol/L, p = 0.39 and 4.86 +/- 1.36 vs. 4.96 +/- 1.41 nmol/L, p = 0.91). In conclusion, our data do not argue in favor of an impairment of beta-cell function at 25 yr of age as a consequence of in utero undernutrition, but rather suggest that insulin resistance might be the primary defect responsible for the development of metabolic disorders associated with IUGR in adulthood.     

糖耐量减低肥胖儿童胰岛素原和真胰岛素水平测定意义

目的　探讨血清胰岛素原 (PI)及真胰岛素 (TI)测定对肥胖并糖耐量异常患儿的临床意义。方法　选择肥胖并糖耐量减低 (IGT)患儿 2 1例 ,肥胖糖耐量正常 (NGT) 5 2例 ,正常对照组 4 0例。测定各组空腹血清PI、TI、血糖 (G)、胰岛素 (I)和C 肽 (C P) ,并计算PI/I、PI/C P、PI/TI及胰岛素抵抗指数。结果　 1.肥胖并IGT和并NGT两组患儿比较 ,G、PI、C P及胰岛素抵抗指数均明显增加 (P均 <0 .0 1)。 2 .IGT组糖尿病阳性家族史明显高于NGT组 (P =0 .0 2 4 )。结论　高PI、高C P和胰岛素抵抗是肥胖并IGT患儿的突出表现 ,可能是儿童2型糖尿病的预示指标。有糖尿病阳性家族史肥胖儿童更应警惕IGT发生     

Familial insulin resistance and acanthosis nigricans

Insulin resistance exists in 0.1% of diabetics having insulin treatment. In addition to diabetics, insulin resistance can also be seen in association with acanthosis nigricans. Both conditions become a syndrome that may happen in a family. This is a report of two siblings, a brother and a sister, 14 and 10 years of age, whose parents are cousins, who suffered from diabetes mellitus, acanthosis nigricans, and growth retardation. The insulin therapy until 54 units per day given to the boy and 174 units per day to the girl, did not give response to the plasma glucose level. Plasma C-peptide and prolactin values of the girl were normal. The plasma fasting insulin level of both was high. Measurement of insulin binding to erythrocytes and monocytes was not performed. The GTT observations of their parents did not represent glucose intolerance.