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。     

不同糖耐量状态肥胖儿童血清脂联素的变化及其临床意义

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(LDL C)、血糖和胰岛素(FINS)，计算胰岛素抵抗指数(HOMA IR)。肥胖组儿童均做口服葡萄糖耐量试验(OGTT)，测定OGTT 2h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，HOMA IR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、LDL C、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。     

脂肪细胞因子与多囊卵巢综合征

多囊卵巢综合征(PCOS)是一种伴有肥胖,胰岛素抵抗的常见代谢性疾病,而脂肪细胞因子在参与肥胖、胰岛素抵抗及相关疾病的发生中起着重要作用.综述近年来研究较多的脂肪细胞因子瘦素、肿瘤坏死因子-α、抵抗素及脂联素在PCOS患者中的表达情况及其作用特点,为PCOS的病因学研究提供新的思路.     

脂肪细胞因子与多囊卵巢综合征

多囊卵巢综合征(PCOS)是一种伴有肥胖，胰岛素抵抗的常见代谢性疾病，而脂肪细胞因子在参与肥胖、胰岛素抵抗及相关疾病的发生中起着重要作用。综述近年来研究较多的脂肪细胞因子瘦素、肿瘤坏死因子-α、抵抗素及脂联素在PCOS患者中的表达情况及其作用特点，为PCOS的病因学研究提供新的思路。     

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。     

与肥胖相关的脂肪细胞因子的研究进展

脂肪细胞因子是脂肪细胞分泌的大量具有活性的物质.现已发现人类脂肪细胞能够分泌瘦素、脂联素、抵抗素等几十种脂肪细胞因子,它们在维持机体能量代谢及内分泌稳态等方面具有显著作用.本文主要阐述脂肪细胞因子与肥胖之间的关系及其可能的机制.     

瘦素、脂联素及抵抗素在多囊卵巢综合征治疗中的变化

目的探讨血脂联素、抵抗素、瘦素及瘦素受体在多囊卵巢综合征(PCOS)抗高雄激素血症治疗和胰岛素增敏剂治疗中的变化.方法27例PCOS患者采用达英-35(每片含醋酸环丙孕酮2mg、炔雌醇35μg)或达英-35联合二甲双胍治疗6个月,ELISA方法检测治疗前后的空腹血脂联素、抵抗素、瘦素及瘦素受体浓度,同时检测血糖和血清胰岛素、双氢睾酮(DHT)、脱氢表雄酮(DHEA)、硫酸脱氢表雄酮(DHEAs)、黄体生成激素(LH)和卵泡刺激素(FSH)等相关激素水平.结果①所有患者的血DHT和DHEA在治疗后均明显降低(P＜0.05);②单用达英-35组治疗后血抵抗素显著下降(P＜0.05),血脂联素升高、瘦素受体降低,但治疗前后差异无显著性,而瘦素没有明显变化;③达英-35联合二甲双胍组治疗后,血脂联素、瘦素受体显著升高,瘦素显著下降(P＜0.05),而抵抗素的下降差异无显著性.结论脂肪细胞分泌的脂联素和瘦素在胰岛素增敏剂治疗后的明显改变,说明其可能参与PCOS胰岛素抵抗的发生发展,而抵抗素的作用尚待研究.     

血清瘦素、抵抗素和脂联素水平与子痫前期的相关性研究

目的探讨瘦素、抵抗素和脂联素这三种脂肪因子的血清浓度与子痫前期发病是否存在相关性。方法采用病例对照研究,所有入组孕妇均来自中国医学科学院北京协和医学院北京协和医院。选取2013年1月至2015年6月期间就诊的74例子痫前期患者为病例组,并根据发病孕周将其分为早发型和晚发型(病例数分别为51例和23例),选取同期产检的无并发症足月分娩孕妇79例为对照组。3种脂肪因子采用酶联免疫吸附法测定。结果病例组和对照组相比,病例组的瘦素水平明显高于对照组[(34.23±22.48)μg/L vs.(15.84±8.98)μg/L,P0.001],瘦素水平在对照组中与BMI呈正相关(r=0.651,P0.001),但在病例组中这种相关性消失;病例组的血清抵抗素水平明显高于对照组[(14.08±6.10)μg/L vs.(9.99±8.33)μg/L,P0.001],抵抗素水平与BMI并无相关性;脂联素水平在两组差异无统计学意义。结论血清抵抗素和瘦素在子痫前期孕妇中明显高于正常妊娠人群,其升高机制仍需进一步探索;脂联素与子痫前期的发生相关性并不明确。     

脂联素与妊娠期糖尿病相关性的研究进展

脂联素(adiponectin)是Scherer等[1]于1995年发现的含244个氨基酸的多肽,基因定位于染色体3q27,全长17 kb,由3个外显子和2个内含子组成.脂联素由脂肪细胞产生并分泌进入血循环,与其他多种脂肪细胞因子(瘦素、肿瘤坏死因子-α、内脂素、抵抗素等)呈负相关,是脂肪细胞因子研究中的新亮点.脂联素可促进血浆游离脂肪酸氧化,增加外周组织对胰岛素的敏感性,在调节糖、脂代谢中起重要作用.     

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。     

超重和肥胖对儿童骨骼强度影响的研究

目的　分析超重和肥胖儿童的骨强度状况。 方法　以2003年10月至2007年1月在首都儿科研究所门诊查体的1270名2～18岁儿童青少年为研究对象, 2～6 岁学龄前儿童按WHO/NCHS身高别体重标准判定超重与肥胖,＞6～18岁学龄儿童根据中国肥胖工作组制定的体重指数（BMI）标准判定超重与肥胖。用Omnisense 7000P型定量超声仪测量骨强度、Genius型体成份仪测量体成份。 结果　学龄前肥胖儿童胫、桡骨骨强度均低于正常儿童,胫、桡骨骨强度下降风险分别是正常 儿童的6.87倍和2.24倍;超重组与正常组无差别。学龄儿童正常、超重、肥胖组的胫骨骨强度依次下降,肥胖、超重组胫骨骨强度下降风险是正常组的9.73和 2.54倍;学龄肥胖组桡骨骨强度低于正常组,超重组与正常组无差别。肥胖儿童不同部位骨强度存在差异。肥胖儿童的体脂含量与骨强度呈负相关（r胫 = -0.35 ; r桡 = -0.33）。 结论　肥胖儿童骨强度较正常儿童差,临床工作中应关注肥胖儿童的骨健康状况,并且应多部位测量以便全面了解骨强度状况。     

北京市7～17岁儿童青少年血压与肥胖状态的关系分析

摘要：目的　探讨北京市7～17岁儿童青少年血压与肥胖状态［依据不同划分标准：体重指数（BMI）、腰围（WC）、体脂百分比（FMP）］的关系。方法　选取2004年4月至10月进行的“北京市儿童青少年代谢综合征研究”（BCAMS）中19 488名7～17岁儿童青少年（男9824名,女9664名）为研究对象,按照BMI、WC、FMP标准分别划分儿童青少年超重和肥胖状态,分析其血压与BMI、WC、FMP关系,高血压状态的变化及趋势。结果　各种划分标准中血压按正常、超重和肥胖组顺序依次升高;控制年龄和性别后,BMI、WC、FMP与收缩压（SBP）和舒张压（DBP）成独立正相关关系（P＜0.001）;BMI、WC、FMP超重组和肥胖组的高血压发生率显著高于正常组,差异有统计学意义（P＜0.001）,肥胖组患高血压的相对危险度是正常组的3～7倍;BMI分组分别与FMP、WC分组组合,BMI肥胖,FMP肥胖组及BMI肥胖,腹型肥胖组患高血压风险分别是正常组的7.3和6.8倍。结论　儿童青少年BMI、WC和FMP与SBP和DBP密切相关,用BMI指标预测儿童青少年高血压风险较WC及FMP更敏感;儿童青少年超重和肥胖增加高血压的发生风险,其高血压发生率随着肥胖程度增加呈现成倍上升趋势。     

Serum adiponectin concentration and cardiovascular risk factors in climacteric women.

OBJECTIVE: Adiponectin plays a significant role in the modulation of glucose tolerance and insulin sensitivity. We attempted to evaluate the relationship between adiponectin level and parameters of the menopausal metabolic syndrome: body mass index, waist-to-hip ratio, lipid profile and insulin resistance indices. SUBJECTS AND METHODS: Thirty-two women and ten men aged 40-63 years were included. The percentage of body fat and of abdominal fat deposits were measured with dual-energy X-ray absorptiometry. Serum adiponectin, tumour necrosis factor-a (TNFalpha) and leptin were measured with commercially available radioimmunoassay kits. To exclude the influence of nutritional factors on adiponectin secretion, diet content was analysed in the preceding three days. RESULTS: Postmenopausal non-obese women had a non-significantly lower level of adiponectin compared with premenopausal women of corresponding body mass. Serum adiponectin level was significantly lower in postmenopausal obese women than in non-obese women (p = 0.0023). Men with similar age and body mass to the women had the lowest level of adiponectin (p = 0.06). Three months of estrogen replacement therapy in women with surgical menopause did not significantly change the serum level of adiponectin. We found a negative correlation of adiponectin with leptin, insulin resistance index and total cholesterol, and a positive correlation with high-density lipoprotein cholesterol. Adiponectin level was negatively correlated with free testosterone, but we did not find such a relationship with estradiol. There was no correlation of adiponectin level with TNFalpha; however, serum TNFalpha correlated positively with leptin. The dietary analysis showed no differences between the diets of obese and non-obese women over the preceding three days. Moreover, mean diastolic and systolic blood pressures were noted to be significantly lower in premenopausal women than in postmenopausal non-obese women (p = 0.05). CONCLUSIONS: Our results suggest that adiponectin could be a marker of risk for developing menopausal metabolic syndrome. Moreover, it is possible that sex steroids have an influence on adiponectin secretion.     

Influence of obesity and menopausal status on serum leptin, cholecystokinin, galanin and neuropeptide Y levels.

Obesity occurs in 60% of women after menopause and is characterized by an excess of adipose tissue that depends on several orexigenic (neuropeptide Y (NPY) stimulates carbohydrate ingestion, galanin stimulates fat intake) and anorectic (leptin, cholecystokinin (CCK)) factors. Both leptin and insulin can reduce hypothalamic NPY production and secretion. Behavior related to the consumption of food is probably attributed to the NPY-galanin signalling route. We investigated basal levels of serum leptin, CCK, galanin and NPY in 16 non-obese premenopausal women, in 15 obese premenopausal women (body mass index (BMI) 34.6 +/- 1.3 SD) and in ten obese postmenopausal women (BMI 34.7 +/- 1.5 SD) to determine the relationship between obesity, menopause and these neuropeptides. Obese premenopausal women had three-fold elevations of serum leptin (32.1 +/- 3.2 ng/ml) in comparison to non-obese premenopausal women (10.3 +/- 1.5 ng/ml), but similar levels to those in obese postmenopausal women (35.3 +/- 4.1 ng/ml). In all 44 patients and in both sub-groups of premenopausal and postmenopausal women, serum leptin exhibited a strong positive correlation with BMI (r = 0.8692, p < 0.0001; r = 0.8803, p = 0.0001; r = 0.8184, p = 0.0001, respectively). Serum galanin values showed a statistically significant increment in the obese postmenopausal group (51.1 +/- 8.1 pg/ml) compared to both premenopausal groups: the non-obese (34.9 +/- 5.8 pg/ml) and the obese (36.0 +/- 5.5 pg/ml). Non-obese menstruating women demonstrated NPY levels (175.0 +/- 12.8 pg/ml) significantly higher than those of obese premenopausal women (126.0 +/- 12.1 pg/ml) and obese postmenopausal women (138.1 +/- 15.4 pg/ml). CCK values showed no differences between non-obese and obese pre- and postmenopausal groups. Basal insulin values were elevated in both obese groups compared to non-obese premenopausal women. Significantly increased leptin and galanin levels in postmenopausal obese women coupled with decreased NPY levels revealed some changes in the neuropeptides regulating eating behavior, which may be the reason for the onset of postmenopausal obesity.     

Association between polycystic ovarian syndrome, overweight, and metabolic syndrome in adolescents

PurposePolycystic syndrome (PCOS) is associated with multiple metabolic abnormalities. Studies in the adolescent population are still limited and the results have been much different. The aim of this study was to investigate the association between PCOS, overweight, and metabolic syndrome in adolescents.Methods30 PCOS adolescents were randomly selected from a PCOS population with NIH 1990 criteria and 71 adolescents from the normal adolescents. Anthropometric, hormonal and metabolic parameters were evaluated in four sub-groups including obese and non-obese PCOS and obese and non-obese normal adolescents.ResultsThe prevalence of overweight and metabolic syndrome in adolescents with PCOS was 52% and 33.3% respectively vs 22.4% (P = 0.005) and 11.26% in control (normal) adolescents (P = 0.0001). Among all subjects, including obese and non-obese adolescents with or without PCOS, the prevalence of insulin resistance, hypercholesterolemia, central obesity, and metabolic syndrome was higher in obese PCOS with 61.5%, 46.2%, 53.8%, and 69.2%, respectively.ConclusionsObesity and IR are important risk factors for metabolic syndrome in PCOS. Considering the long-term health risks, it is necessary to identify metabolic disorders in adolescents with PCOS as early as possible.     

血清抵抗素、C-反应蛋白及IL-6与PCOS的相关性研究

目的:探讨血清脂肪细胞因子抵抗素(resistin)、C-反应蛋白(CRP)、白细胞介素6(IL-6)水平与PCOS发生的相关性。方法:收集PCOS患者45例,再根据体质量指数(BMI)分为肥胖亚组(≥25kg/m2,22例)和非肥胖亚组(<25kg/m2,23例)。正常对照组45例,同样按BMI分为肥胖亚组(14例)和非肥胖亚组(31例)。空腹采集血清,采用酶联免疫分析法测定抵抗素、免疫比浊法测定CRP、放射免疫法测定IL-6,全自动生化分析仪测定血糖、血脂、化学发光法测定内分泌水平和血清胰岛素水平,同时测量身高、体质量、腰围、臀围,计算BMI和腰臀比值(WHR)。结果:与对照组非肥胖者相比,PCOS组肥胖、非肥胖者及对照组肥胖者抵抗素水平均显著增高(P<0.05);PCOS组和对照组肥胖者的CRP水平均高于对照组非肥胖者(P<0.05);PCOS组肥胖和非肥胖者的IL-6水平高于对照组非肥胖者(P<0.05)。抵抗素和CRP均与BMI、WHR、HOMA-IR呈显著正相关(P<0.05);IL-6与BMI、WHR有显著相关性,与HOMA-IR无相关性。结论:脂肪细胞因子抵抗素、CRP及IL-6参与PCOS患者肥胖和胰岛素抵抗的发生发展。     

Serum adiponectin concentration and cardiovascular risk factors in climacteric women

Objective Adiponectin plays a significant role in the modulation of glucose tolerance and insulin sensitivity. We attempted to evaluate the relationship between adiponectin level and parameters of the menopausal metabolic syndrome: body mass index, waist-to-hip ratio, lipid profile and insulin resistance indices.

Subjects and methods Thirty-two women and ten men aged 40–63 years were included. The percentage of body fat and of abdominal fat deposits were measured with dual-energy X-ray absorptiometry. Serum adiponectin, tumour necrosis factor-α (TNFα) and leptin were measured with commercially available radioimmunoassay kits. To exclude the influence of nutritional factors on adiponectin secretion, diet content was analysed in the preceding three days.

Results Postmenopausal non-obese women had a non-significantly lower level of adiponectin compared with premenopausal women of corresponding body mass. Serum adiponectin level was significantly lower in postmenopausal obese women than in non-obese women (p?=?0.0023). Men with similar age and body mass to the women had the lowest level of adiponectin (p?=?0.06). Three months of estrogen replacement therapy in women with surgical menopause did not significantly change the serum level of adiponectin. We found a negative correlation of adiponectin with leptin, insulin resistance index and total cholesterol, and a positive correlation with high-density lipoprotein cholesterol. Adiponectin level was negatively correlated with free testosterone, but we did not find such a relationship with estradiol. There was no correlation of adiponectin level with TNFα; however, serum TNFα correlated positively with leptin. The dietary analysis showed no differences between the diets of obese and non-obese women over the preceding three days. Moreover, mean diastolic and systolic blood pressures were noted to be significantly lower in premenopausal women than in postmenopausal non-obese women (p?=?0.05).

Conclusions Our results suggest that adiponectin could be a marker of risk for developing menopausal metabolic syndrome. Moreover, it is possible that sex steroids have an influence on adiponectin secretion.     

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。     

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