孕妇肥胖对婴儿体格发育和瘦素质量浓度的影响

目的探讨孕妇肥胖对婴儿体格发育和瘦素质量浓度的影响。 方法武汉大学人民医院儿科于2002年1月至2003年6月选择肥胖孕妇和正常体重孕妇各80例,比较她们的子代在出生后及满1岁时的体重、身高和血清瘦素质量浓度；瘦素检测使用双抗体夹心ELISA法。 结果符合检测数据统计条件的肥胖组为53例，正常组49例。(1)肥胖孕妇的瘦素质量浓度明显高于正常体重孕妇(P<0.01)；(2)肥胖孕妇组子代出生体重和脐血瘦素质量浓度明显高于正常组(P<0.01)；(3)肥胖孕妇组子代1岁时体重和血清瘦素质量浓度明显高于正常组子代(P<0.05)。 结论孕妇肥胖对婴儿的体重和瘦素质量浓度有明显的影响，此影响对子代以后的生长发育和瘦素质量浓度是否继续存在还需要进一步的研究。     

二甲双胍对高胰岛素血症肥胖儿童糖代谢和血清脂源性激素的影响

目的观察二甲双胍治疗对高胰岛素血症肥胖患儿血清脂源性激素脂联素、抵抗素、瘦素水平的影响。 方法2004 01—2005 02将武汉市儿童医院和同济医院54例高胰岛素血症肥胖患儿分为轻、中度肥胖组及重度肥胖组,均以二甲双胍治疗12周，测量治疗前后体重、空腹血糖、空腹胰岛素及脂源性激素脂联素、瘦素、抵抗素的变化。 结果治疗前轻、中度肥胖组和重度肥胖组高胰岛素血症患儿空腹血糖水平与健康对照组比较差异无显著性(P>0.05)，血清胰岛素、瘦素、抵抗素及胰岛素抵抗指数(HOMA IR)均高于健康对照组(P<0.01)，脂联素水平明显低于健康对照组(P<0.01)。二甲双胍治疗12周后与治疗前相比,血清胰岛素水平、胰岛素抵抗指数明显降低(P<0.01)，轻、中度肥胖组及重度肥胖组血清瘦素水平分别由治疗前的(24.3±1.8)μg/L、(30.2±5.1)μg/L降低为治疗后的(19.6±6.3)μg/L、(24.7±5.3)μg/L，差异有统计学意义；抵抗素水平分别由治疗前的(16.5±6.0)μg/L、(22.3±5.2)μg/L升高为(22.0±5.1)μg/L、(30.6±11.7)μg/L，差异有统计学意义；轻、中度肥胖组和重度肥胖组血清脂联素水平治疗前分别为(8.4±3.2)mg/L、(6.5±1.2)mg/L，治疗后分别为(8.9±2.3)mg/L、(7.03±3.0)mg/L，治疗前后相比,P>0.05。体重指数(BMI)下降,但差异无显著性。 结论二甲双胍能显著改善肥胖患儿胰岛素抵抗。降低血清瘦素水平可能是其改善胰岛素抵抗机制之一，但在对脂源性激素脂联素、抵抗素水平的改善上，有其局限性。     

血清脂联素水平测定在多囊卵巢综合征中的意义

目的:探讨脂联素水平在多囊卵巢综合征(PCOS)中的意义。方法:选择我院PCOS患者48例作为研究对象,同期选择非PCOS患者40例作为对照,分为肥胖组与非肥胖组,胰岛素抵抗组与非胰岛素抵抗组。测定血清脂联素水平及内分泌代谢指标。结果:①PCOS组血清脂联素水平低于对照组(P<0.05);非肥胖PCOS组低于非肥胖对照组(P<0.05);胰岛素抵抗组低于非胰岛素抵抗组(P<0.05)。②血清脂联素水平与体重指数(BMI)、空腹胰岛素(FINS)、胰岛素抵抗指数(HOMA-IR)、腰臀比(WHR)、甘油三酯(TG)呈负相关(P<0.01,P<0.05),与葡萄糖胰岛素比值(GIR)、胰岛素敏感指数(ISI)呈正相关(P<0.01)。控制BMI影响后血清脂联素水平仍与HOMA-IR、TG呈负相关(P<0.05),与GIR、ISI呈正相关(P<0.01)。结论:①PCOS患者存在低脂联素血症,脂联素水平与胰岛素抵抗程度呈负相关。②脂联素可以作为PCOS发生糖尿病远期并发症的预测指标。     

肥胖与非肥胖多囊卵巢综合征患者血清肿瘤坏死因子-α(TNF-α)水平的比较

目的:比较肥胖与非肥胖多囊卵巢综合征(PCOS)患者血清肿瘤坏死因子-α(TNF-α)水平的差异。方法:55例PCOS患者,根据体质量指数(BMI)分为肥胖组(BMI>25,n=31)和非肥胖组(BMI≤25,n=24);同期选择50例非PCOS育龄妇女,分为肥胖对照组(BMI>25,n=25)和非肥胖对照组(BMI≤25,n=25)。应用酶联免疫吸附法(ELISA)测定血清TNF-α的含量,分析TNF-α与胰岛素抵抗指数(HOMA-IR)的相关性。结果:PCOS肥胖组与PCOS非肥胖组的TNF-α水平分别显著高于其相应的对照组(P<0.01),PCOS非肥胖组的TNF-α水平也显著高于肥胖对照组(P<0.05)。PCOS肥胖组与PCOS非肥胖组之间的TNF-α水平无显著差异(P>0.05)。PCOS组TNF-α与HOMA-IR呈显著正相关(P<0.05)。结论:肥胖与非肥胖PCOS患者的血清TNF-α水平均升高,可能存在肥胖以外升高TNF-α的途径;TNF-α与PCOS的IR发生有密切联系。     

肥胖症儿童血浆脂联素与胰岛素抵抗的相关性

目的探讨血清脂联素水平与高胰岛素血症和(或)胰岛素抵抗的联系。 方法采用酶联免疫法测定2004-02—2004-12在天津医科大学总院就诊的34例肥胖儿童和31例正常对照的血清脂联素水平。分析血清脂联素与人体参数、体脂分布及糖代谢中各指标的相关关系。 结果(1)肥胖组脂联素水平低于对照组(P<0001)。(2)脂联素与性别、年龄无相关关系；与收缩压、舒张压呈负相关(相关系数分别为r=-0369，r=-0405，P<001)；与BMI、腰臀比和SF呈负相关(相关系数分别为r=-0330，r=-0282和r=-0350，P<001)；与空腹血糖、空腹胰岛素水平呈负相关(相关系数r=-0264和r=-0357，P<001)；与HOMA R呈负相关(P<001)，与HOMA β无相关关系。(3)多元回归分析表明，HOMA R是影响脂联素最为显著的因素，R2=0122；标准化偏回归系数-0369(P<001)。 结论肥胖症儿童血清脂联素水平较正常儿童降低。血清脂联素水平的变化，是影响空腹血糖、空腹胰岛素水平、HOMA R的重要因素。低脂联素血症可能参与胰岛素抵抗的发生。     

卵巢黄素化颗粒细胞瘦素信号转导分子STAT3磷酸化在多囊卵巢综合征发病中的作用

目的:探讨瘦素在多囊卵巢综合征(PCOS)发病中的作用。方法:选择行IVF-ET治疗的30例PCOS患者根据体重指数(BMI)分为肥胖者(BMI≥24)15例和非肥胖者(BMI<24)15例,及同期排卵功能正常或单纯输卵管因素不孕的非PCOS肥胖者和非肥胖者各15例,采用ELISA检测各组血清瘦素水平;采用放射免疫法检测各组空腹血清胰岛素(FIN)水平;采用葡萄糖氧化酶法测定各组空腹血糖(FPG)水平,利用稳态模型(HOMA)计算胰岛素抵抗指数(即HOMA-IR);采用Western blotting检测卵巢黄素化颗粒细胞信号转导分子STAT3磷酸化水平;同法检测不同浓度的瘦素(0ng/ml、10ng/ml、100ng/ml、1000ng/ml)体外对正常人卵巢黄素化颗粒细胞STAT3磷酸化(p-STAT3)的影响。结果:①血清瘦素水平PCOS肥胖者最高,其后依次为对照组肥胖者、PCOS非肥胖者和对照组非肥胖者,各组之间两两比较,差异均具有显著性(P<0.05);②PCOS患者血清瘦素水平与BMI和HOMA-IR均呈显著正相关(r=0.707,P<0.01;r=0.761,P<0.01);③STAT3水平肥胖PCOS组最高,其后依次为肥胖对照组、非肥胖PCOS组和正常对照组,各组间两两比较,差异均具有显著性(P<0.05);④正常人卵巢黄素化颗粒细胞经不同浓度瘦素处理48h后,p-STAT3水平呈不同程度增加,至瘦素浓度达到100ng/ml时,p-STAT3水平达到高峰,随后呈下降趋势。结论:瘦素可能通过激活JAK2/STAT3信号传导通路参与PCOS排卵障碍的发生。     

血清胰岛素浓度的变化与肥胖儿童生长关系的探讨

目的探讨单纯性肥胖儿童的生长与其血清胰岛素(Ins)、胰岛素样生长因子 1(IGF 1)、胰岛素样生长因子结合蛋白 3(IGFBP 3)浓度的关系。 方法2004 03中山大学附属二院对31例单纯性肥胖儿童及48例同龄正常儿童的生长参数及空腹Ins、IGF 1、IGFBP 3浓度进行测定，并进行比较及相关性分析。 结果肥胖组血清Ins、IGFBP 3浓度显著高于对照组(P<005,P<001)，而两组间IGF 1差异则无显著性意义，血清Ins浓度与BMI、IGFBP 3呈正相关，肥胖儿童身高SDS与1NS、IGF 1正相关。 结论肥胖儿童存在有非生长激素(GH)依赖性生长的代偿机制。其中高胰岛素血症可能参与了这一过程，它既可以通过增加IGFBP 3的合成来间接提高IGF 1的生物活性，又可以直接发挥促生长作用。     

妊娠期糖尿病患者血清瘦素肿瘤坏死因子与胰岛素抵抗的关系

目的探讨妊娠期糖尿病患者血清瘦素(Leptin)与胰岛素抵抗水平、肿瘤坏死因子的关系。方法2002年1月至2005年2月解放军181医院对32例妊娠期糖尿病患者(GDM)为观察组,随机选择同期门诊及住院36例糖耐量正常妊娠妇女为对照组,均进行75g葡萄糖耐量试验(OGTT),同时测定空腹血清瘦素(leptin)、肿瘤坏死因子(INFα)、胰岛素(FINS),稳态模型(HOMA)计算胰岛素抵抗指数(HOMAIR),并应用pearson分析妊娠期糖尿病患者胰岛素抵抗与瘦素、INFα、空腹胰岛素、体重指数(BMI)的关系。结果观察组血清瘦素、INFα、FINS及胰岛素抵抗指数均明显高于对照组(P<0.05或P<0.01);血清瘦素、INFα、FINS、BMI与HOMAIR呈正相关(P<0.01)。结论瘦素、肿瘤坏死因子是影响妊娠期糖尿病患者胰岛素抵抗的重要因素之一。     

妊娠期糖尿病患者血清网膜素水平与糖、脂代谢指标的相关性研究

目的:探讨妊娠期糖尿病(GDM)患者血清网膜素(Omentin)水平的变化及其与糖、脂代谢指标的相关性。方法:采用酶联免疫吸附法检测35例孕前肥胖的GDM孕妇(A组)、32例孕前非肥胖的GDM孕妇(B组)、36例正常健康孕妇(C组)的血清Omentin水平;同时测定所有受试者的糖、脂生化指标,并计算胰岛素抵抗指数(HOMA-IR)。结果:(1)GDM孕妇三酰甘油(TG)、空腹血糖(FPG)、空腹胰岛素(FINS)、胰岛素抵抗指数(HOMA-IR)水平均高于正常对照组,高密度脂蛋白(HDL-C)水平低于正常对照组(P均<0.05);(2)3组孕妇血清Omentin水平A组相似文献   

单纯性肥胖外周血单核/巨噬细胞趋化因子与胰岛素抵抗的相关性研究

了解单纯性肥胖儿童外周血单核/巨噬细胞趋化因子与胰岛素抵抗相关参数的关系。方法　2006年5月至2008年5月广西医科大学第一附属医院儿科70 例确诊为单纯性肥胖儿童作为研究对象,30名健康体检儿童作为健康对照组。流式细胞仪测定外周血单核细胞CD68阳性率;酶联免疫吸附（ELISA）法测定血浆巨 噬细胞炎性蛋白-1α（MIP-1α）、单核细胞趋化蛋白-1（MCP-1）水平;放射免疫分析（RIA）法测定血浆脂联素（ADPN）、血浆胰岛素（Ins）浓度,计算体质 指数（BMI）,按HOMA模型计算胰岛素抵抗指数（InRI）,并与相关变量进行Pearson相关分析或偏相关分析。结果　单纯性肥胖组血浆MIP-1α、MCP-1水平高于 健康对照组,两组比较差异有统计学意义（P < 0.05）。两组外周血CD68阳性率比较差异无统计学意义（P > 0.05）。两组InRI比较差异有统计学意义 （P < 0.05）。单纯性肥胖组血浆MIP-1α、MCP-1水平分别与BMI、腰围（WC）和InRI呈正相关 （P < 0.05）。血ADPN分别与BMI、WC和InRI呈负相关（P < 0.05）。外 周血单个核细胞CD68阳性率与BMI、WC和InRI无相关性（ P > 0.05）。结论　单纯性肥胖患儿体内存在低程度炎症反应,肥胖儿童外周血单核/巨噬细胞趋化因子 与胰岛素抵抗及中心性肥胖相关,可以作为肥胖相关疾病的早期预测指标之一。     

Serum leptin levels correlate with obesity parameters but not with hyperinsulinism in women with polycystic ovary syndrome

OBJECTIVE: To examine serum leptin concentrations in obese and lean patients with polycystic ovary syndrome (PCOS) to assess whether the changes in leptin levels are due to obesity or hormonal alterations. DESIGN: Controlled clinical study. SETTING: Academic research environment. PATIENT(S): Obese and lean women with PCOS. INTERVENTION(S): Blood samples were collected before and after food consumption. MAIN OUTCOME MEASURE(S): Serum leptin and insulin levels. RESULT(S): Serum leptin concentrations were significantly correlated with body mass index (r = 0.649) and also with HOMA (r = 0.535). However, after controlling for body mass index in a partial correlation analysis, no significant correlation was found between serum leptin levels and HOMA or hyperinsulinemia. While lean patients with PCOS had a significant correlation between leptin concentrations and obesity parameters, they did not show any significant correlation with insulin resistance parameters. CONCLUSION(S): Although leptin concentrations in women with PCOS correlate with insulin resistance/hyperinsulinemia, this is related only to obesity.     

Serum leptin levels correlate with clinical and biochemical indices of insulin resistance in women with polycystic ovary syndrome

Objectives To compare serum leptin levels in women with polycystic ovary syndrome (PCOS) and healthy subjects, and to evaluate the relationship between leptin concentration and insulin resistance.

Methods Forty-five women with PCOS and 20 controls were included in the study. Serum levels of leptin, testosterone, immune-reactive insulin (IRI), sex hormone-binding globulin, dehydroepiandrosterone sulfate, cortisol, LH and FSH were measured. Free androgen index (FAI) and homeostasis model assessment of insulin resistance (HOMA-IR) were calculated. Body mass index (BMI) and waist-to-hip ratio (WHR) were assessed.

Results Serum leptin levels in PCOS patients were higher than in the control group independently of BMI, WHR and waist circumference. In PCOS patients there was a strong positive correlation between leptin and IRI (r = 0.592, p < 0.01) on the one hand, and leptin and HOMA-IR, on the other (r = 0.637, p < 0.01). In PCOS patients with more pronounced insulin resistance (IR) the correlation between leptin levels and HOMA-IR is independent of BMI, WHR and waist circumference. We did not find any correlation between leptin and other hormonal indices in PCOS patients.

Conclusions Our study confirms the existence of a significant positive correlation between serum leptin levels and clinical and hormonal indices of IR. The hyperleptinaemia is probably due to leptin resistance and may be characteristic of the syndrome. The lack of correlation with other hormonal parameters is probably due to the heterogeneity of the PCOS group.     

Neuropeptide Y, leptin, galanin and insulin in women with polycystic ovary syndrome.

It has been reported that polycystic ovary syndrome (PCOS) is very frequently associated with obesity, insulin resistance and hyperinsulinemia. However, metabolic disorders may lead to suppression of reproductive hormone secretion during undernutrition and in obesity. Some neuropeptides, such as neuropeptide Y (NPY) and galanin, modulate the control of appetite and play an important role in the mechanism of luteinizing hormone-releasing hormone (LHRH) secretion. NPY and galanin regulate appetite via both central and peripheral mechanisms. The interaction between central and peripheral signals for the control of food intake is due to leptin. Leptin can modulate the activity of NPY and other peptides in the hypothalamus that are known to affect eating behavior. In order to evaluate the relationship between NPY, galanin and leptin, 28 women with PCOS, 32 obese women (non-PCOS) and 19 lean healthy women (control group) were investigated. Obese women with PCOS were divided into two groups: PCOS (A) overweight (body mass index, BMI 26-30 kg/m2), and PCOS (B) obese (BMI 31-40 kg/m2). Plasma NPY, galanin and leptin concentrations were measured by radioimmunoassay. Plasma leptin levels in obese women with PCOS (groups A and B) were significantly higher than those in the control group (p < 0.05, p < 0.05, respectively). A significant positive correlation between plasma leptin and BMI in women with PCOS was found (r = 0.427, p < 0.01). A positive correlation was demonstrated between leptin and testosterone in PCOS (r = 0.461, p < 0.01). Plasma galanin concentrations in PCOS were higher than in the control group but the differences were not significant. Plasma NPY levels were significantly elevated in both non-obese (normal) and obese women with PCOS (group A) (p < 0.01, p < 0.005, respectively). However, in obese non-PCOS women plasma NPY levels gradually increased with increase in BMI. No significant correlations were found between galanin, NPY and percentage change in response of LH to LHRH, as well as between NPY and insulin, and galanin and testosterone. Plasma insulin concentrations in women with PCOS (group B) were significantly higher than in the control group (p < 0.001). Increased plasma NPY levels are found in both obese and non-obese women with PCOS. The increase in NPY is independent of the increase in BMI. In obese women with PCOS, plasma leptin is increased compared with control lean women. Serum insulin concentration is increased in obese women with PCOS. A positive correlation exists between leptin and BMI as well as between leptin and testosterone in women with PCOS. These results may suggest that the feedback system in the interaction between leptin and NPY is disturbed in PCOS.     

性早熟女童糖脂代谢与脂联素的关系

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。     

Sumac (Rhus coriaria L.) powder supplementation has beneficial effects on appetite in overweight/obese women with depression: A randomized controlled trial

Background and purposeAppetite disturbance is a common problem in obesity and depression. The beneficial effects of polyphenols in promoting satiety have been shown. This study aimed to investigate the effects of sumac supplementation along with calorie restricted diet (CRD) on appetite in overweight and obese women with depression.Materials and methodsIn this trial, 60 overweight and obese women with depression were randomly assigned to receive a CRD plus 3 g/day of either sumac or placebo for 12 weeks. The appetite score, serum levels of leptin, neuropeptide Y (NPY), insulin, fasting blood sugar (FBS), homeostasis model assessment of insulin resistance (HOMA-IR), and quantitative insulin sensitivity check index (QUICKI) were assessed at baseline and at the end of the study.ResultsSumac supplementation significantly reduced the appetite score (p = 0.02), serum levels of leptin (p = 0.03), NPY (p = 0.01), insulin (p = 0.03), FBS (p = 0.03), and HOMA-IR (p = 0.02) compared to the placebo group. QUICKI increased significantly in the sumac group compared to the placebo group (p = 0.009).ConclusionSumac along with a CRD may have some beneficial effects on appetite through possible modulatory effects on leptin resistance, insulin sensitivity, and NPY levels in overweight and obese women with depression.     

Are serum chemerin levels different between obese and non-obese polycystic ovary syndrome women?

The objective of this study is to measure serum chemerin levels in women with polycystic ovary syndrome (PCOS) and assess their relationship with clinical, metabolic, and hormonal parameters. One hundred eighteen PCOS women and 114 healthy women were recruited in this study. Their blood pressure, body mass index (BMI), waist circumference and waist-to-hip ratio (WHR), fasting insulin (FIN), fasting plasma glucose (FPG), blood serum sex hormone, and blood lipid were measured. Serum chemerin, leptin, and adiponectin were measured by ELISA. Serum chemerin was significantly higher in the obese PCOS group (47.62?±?11.27?ng/mL) compared with non-obese PCOS (37.10?±?9.55?ng/mL) and the obese (33.71?±?6.17?ng/mL) and non-obese (25.78?±?6.93?ng/mL) control groups (p?p?相似文献   

多囊卵巢综合征血浆瘦素的改变及相关影响因素的研究

目的探讨多囊卵巢综合征(PCOS)患者血浆瘦素(leptin)水平的变化及其相关影响因素。方法用放射免疫学方法检测63例PCOS患者血浆leptin、血清泌乳素、促黄体生成素、卵泡刺激素、雌二醇、睾酮、雄烯二酮水平,同时行糖耐量及胰岛素释放实验。用相关分析探讨leptin与体重指数(BMI)、性激素、血糖、胰岛素和胰岛素敏感指数的关系。结果PCOS患者空腹胰岛素(r=0.6,P<0.01)和BMI(r=0.351,P<0.01)与血浆瘦素呈显著正相关,且空腹胰岛素对瘦素的影响更显著。结论瘦素可能与PCOS的胰岛素抵抗、高胰岛素血症密切相关。     

肥胖儿童载脂蛋白E基因型与临床表现的相关性

目的探讨单纯性肥胖儿童载脂蛋白(apolipoprotein,Apo)E基因多态性的分布及其对血脂、脂蛋白、载脂蛋白的影响，及其与冠状动脉、心电图改变的关系。并对其早期预测和疾病预防提供理论依据。 方法选择2002年12月至2004年12月潍坊医学院附属医院儿科的6~14岁单纯性肥胖儿童89例和健康儿童76例。抽取外周静脉血，测定血清中甘油三酯(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)，载脂蛋白A1(Apo A1)，载脂蛋白B100(Apo B100)浓度。应用改良的聚合酶链式反应 限制性片段长度多态性(PCR RFLP)分析及聚丙烯酰胺凝胶电泳测定儿童Apo E基因型。 结果共检出4种Apo E基因型，E3/3、E4/3、E2/3、E4/2，以ε3为最常见。与健康儿童比较，肥胖儿童ε4等位基因频率增高，差异有显著性(P<005)。 结论单纯性肥胖儿童有Apo E基因多态性的变化，且明显影响小儿血浆脂类代谢，肥胖儿童Apo E4与冠心病有密切相关性。