上海地区汉族健康人群血清脂联素水平分析

目的探讨上海地区汉族健康人群血清脂联素水平，分析其与年龄、性别、血脂浓度及胰岛素抵抗指数的关系。方法收集400名汉族健康体检者的血清标本，采用酶联免疫吸附双抗夹心（ELISA）法测定血清脂联素水平和血清空腹胰岛素（FINS）水平。结果上海地区汉族健康人血清空腹脂联素水平为（9．48±4．86）μg／ml，各年龄组间比较差异无统计学意义；男性脂联素浓度为（8．46±3．97）μg／ml，女性为（10．22±5．30）μg／ml，男性和女性相比脂联素浓度差异有统计学意义；女性绝经前后脂联素浓度分别为（11．89±4．78）μg／ml和（8．78±4．65）μg／ml，两者脂联素浓度差异有统计学意义。结论①血清脂联素浓度在各年龄段差异无统计学意义；女性脂联素浓度高于男性，差别有统计学意义（P〈0．05）；绝经前、后女性脂联素浓度差异有统计学意义（P〈0．05）。②血清脂联素水平与空腹胰岛素水平、体重、体重指数、腰臀比、收缩压、LDL—C等指标呈负相关，与HDL—C水平呈正相关。     

高血压患者胰岛素抵抗与血清脂联素及炎症标志物水平

目的探讨高血压患者胰岛素抵抗与血清脂联素水平及炎症标志物变化的关系。方法入选非糖尿病的新发高血压患者108例，同时入选64例血压正常者作为对照。常规检测受试者的血压、血糖、血脂和胰岛素，计算稳态模型胰岛素抵抗指数（HOMA-1R），同时检测血清脂联素、高敏C反应蛋白（hs-CRP）、肿瘤坏死因子α（TNF-α）、白介素6（IL-6）及可溶性E选择素（sE-s）。根据血压水平对患者进行分组，比较各组血清脂联素及炎症标志物水平的差异；用logistic回归筛选平均动脉压的影响因素。结果1）HOMA-IR随着血压的升高而升高，2级和3级高血压患者与对照组比较差异有统计学意义（P〈0．05）；2）总体高血压患者血清脂联素水平（4．5±2．0）mg／L低于对照组（7．1±1．9）mg／L，炎症标志物hs-CRP、TNF-α、IL-6和sE-s水平高于对照组，（P均〈0．01）；3）相关分析显示脂联素与收缩压、舒张压、HOMA-IR、hs-CRP、TNF-α、IL-6和sE-s呈负相关，相关系数分别为-0．533、-0．364、-0．375、-0．234、-0．509、-0．416和-0．297（P〈0．05）；4）Logistic回归显示HOMA-IR、hs-CRP、脂联素和BMI是平均动脉压独立的影响因素（P〈0．05）。结论高血压患者血清脂联素水平低，炎症标志物水平高，存在胰岛素抵抗；随着血压水平的升高，血清脂联素水平逐渐降低，炎症标志物水平逐渐升高，胰岛素抵抗程度加重；HOMA-IR、hs-CRP、脂联素和BMI是平均动脉压独立的影响因素。     

高血压前期与胰岛素抵抗、血清脂联素水平的相关研究

目的探讨人群胰岛素抵抗及血清脂联素水平与高血压前期的关系。方法入选160例体检人群,分为理想血压组（43例）、高血压前期组（79例）、1级高血压组（38例）,分别检测受检者血清脂联素、空腹血清胰岛素水平,采用HOMA-IR法计算胰岛素抵抗指数。对理想血压是否进展为高血压前期进行二分类Lo-gistic回归分析。结果理想血压组、高血压前期组、1级高血压组胰岛素抵抗指数分别为（1.39±0.06）、（1.78±0.06）、（2.49±0.15）,三组间差异有显著统计学意义（P〈0.01）。高血压前期组、1级高血压组血清脂联素水平分别为（17.76±0.99）mg/L、（18.59±1.32）mg/L,两组差异无统计学意义;两组血清联素水平与理想血压组[（22.89±1.25）mg/L]比较,差异均有显著统计学意义（P均〈0.01）。Logistic回归分析表明体质指数、胰岛素抵抗指数为理想血压进展为高血压前期的危险因素而脂联素为保护因素。结论高血压前期人群胰岛素抵抗水平已经升高,并伴随脂联素水平下降。     

原发性高血压患者血清脂联素水平及与血压、胰岛素抵抗的关系

目的探讨原发性高血压患者血清脂联素水平及其与血压、胰岛素抵抗之间的关系。方法选取原发性高血压患者65例及健康对照者40名,用酶联免疫吸附法检测各组空腹血清脂联素浓度,同时测定各组的血压、体重指数、腰围、血糖、胰岛素等指标,采用稳态模型法计算胰岛素抵抗指数(IRI)和胰岛素敏感指数(ISI),并分析血清脂联素与各指标间的相关性。结果原发性高血压组血清脂联素水平显著低于健康对照组[(10.30±0.93)μg/ml比(12.83±1.66)μg/ml),P=0.000]。Pearson相关性分析显示,原发性高血压组血清脂联素与收缩压(r=-0.304,P=0.032)、体重指数(r=-0.496,P=0.000)、腰围(r=-0.539,P=0.000)、空腹胰岛素(r=-0.291,P=0.040)、IRI(r=-0.334,P=0.018)之间呈负相关,与ISI呈正相关(r=0.297,P=0.037)。多元逐步回归分析显示,收缩压、腰围是影响脂联素水平的独立危险因素。结论原发性高血压患者血清脂联素水平下降,且与收缩压、胰岛素抵抗具有一定的相关性。     

妊娠期糖尿病患者分娩前后血清脂联素和胰岛素样生长因子-1的变化

目的探讨妊娠期糖尿病患者分娩前后血清脂联素、胰岛素样生长因子．1的变化。方法入选76例育龄妇女,其中31例为正常糖耐量非妊娠女性（G0）,34例为正常糖耐量妊娠女性（G1）,18例为妊娠期糖尿病患者（G2）。在妊娠24周和分娩后6周检测空腹血糖、空腹胰岛素、血清脂联素和胰岛素样生长因子-1。采用稳态模式评估胰岛素抵抗和胰岛13细胞功能。结果分娩前G0组血清脂联素水平高于G1组和G2组（P〈0．05）,但脂联素水平在G1组及G2组间比较差异无统计学意义（P〉0．05）。分娩后G1组血清胰岛素样生长因子．1水平较分娩前明显降低,而血清脂联素水平则明显升高（P〈0．01）。G2组分娩后脂联素水平低于G1组（P〈0．05）。结论妊娠妇女血清脂联素水平下降,尤其是妊娠期糖尿病患者下降更明显。而分娩后血清脂联素有所恢复,低脂联素与胰岛素抵抗密切相关。     

原发性高血压患者血清脂联素浓度的变化及肾素-血管紧张素系统对其影响

目的:探讨原发性高血压患者血清脂联素浓度的变化及肾素-血管紧张素系统对血清脂联素的影响.方法:本研究入选原发性高血压患者60例及健康人30例(正常对照组),以正常对照组人群胰岛素敏感性指数(ISI)的均数±标准差作为有无胰岛素抵抗的分界线,将原发性高血压患者分成两组,即胰岛素抵抗组23例及无胰岛素抵抗组37例.检测血清脂联素、空腹血糖、血清胰岛素、总胆固醇、高密度脂蛋白胆固醇、甘油三酯、胰岛素敏感性指数、收缩压、舒张压、平均压、身高、体重及体重指数等指标.另外,从60例原发性高血压患者中选出能够完成整个实验,积极配合随访的40例患者,并分成两部分,每部分20例,分别用血管紧张素转换酶抑制剂培哚普利及血管紧张素Ⅱ受体拮抗剂缬沙坦治疗两周,治疗前、后检测上述指标.结果:①胰岛素抵抗组的血清胰岛素和甘油三酯与正常对照组及无胰岛素抵抗组相比,胰岛素抵抗组明显升高(P＜0.01),胰岛素抵抗组的脂联素和胰岛素敏感性指数与正常对照组及无胰岛素抵抗组相比,胰岛素抵抗组明显降低(P＜0.01).②高血压患者用培哚普利及缬沙坦治疗两周后,平均压显著下降(P＜0.05),血清脂联素浓度和胰岛素敏感性指数明显升高(P＜0.05).③原发性高血压患者血清脂联素与收缩压和舒张压呈直线相关(r分别为0.35和0.28,P＜0.01和P＜0.05);血清脂联素与胰岛素敏感性指数和高密度脂蛋白胆固醇呈直线相关(r分别为0.45和0.53,P均＜0.01);血清脂联素与血清胰岛素、体重指数及甘油三酯负相关(r分别为-0.41,-0.61和-0.35,P＜0.01,P＜0.01和P＜0.05);血清脂联素与平均压无明显相关性.结论:原发性高血压患者低脂联素血症与脂代谢紊乱和胰岛素抵抗密切相关.肾素-血管紧张素系统,可提高原发性高血压患者胰岛素敏感性,从而使血清脂联素浓度升高.     

妊娠糖尿病患者脂联素与胰岛素抵抗相关性的初步探讨

目的探讨妊娠糖尿病（GDM）患者脂联素与胰岛素抵抗（IR）的关系。方法检测40例GDM患者（GDM）、34例糖耐量正常（NGT）的孕妇作对照（NC）组的血清脂联素水平，同时以稳态模型HOMA-IR计算胰岛素抵抗指数。结果（1）GDM组脂联素水平、HOMA-IR分别为7．83±1．57μg／L，3．57±1．27，对照组分别为9．36±1．41μg／L、2．98±1．03，两组比较差异有统计学意义。（2）GDM组多元线性逐步回归分析结果显示孕前BMI、脂联素是影响GDM患者IR的独立危险因素。结论GDM患者血清脂联素减少与IR密切相关。     

血清脂联素水平在磺脲类药物继发性失效的2型糖尿病患者中的变化及临床意义

目的观察磺脲类降糖药（SU）继发性失效2型糖尿病患者血清脂联素水平与血糖控制良好2型糖尿病患者及正常人之间的差异。方法采用ELISA法检测所有受试者血清脂联素水平,同时检测血糖和血脂,计算体重指数,进行相关性分析。结果血糖控制良好的患者脂联素明显低于正常人（P〈0．05）,SU继发性失效的患者明显低于血糖控制良好的患者（P〈0．05）;两组2型糖尿病患者胰岛素抵抗水平均明显高于正常人（P均〈0．05）,而两组患者比较无明显差异（P〉0．05）。SU继发性失效患者脂联素水平与空腹血糖、餐后2小时血糖、糖化血红蛋白、体重指数、空腹胰岛素、胰岛素抵抗指数、胆固醇、总甘油三酯及低密度脂蛋白胆固醇呈明显负相关（P均〈0．05）,与高密度脂蛋白胆固醇呈明显正相关（P〈0．05）。结论脂联素水平下降和胰岛素抵抗相互影响,可能参与了2型糖尿病SU继发性失效的发生发展。     

胰岛素联合罗格列酮治疗T2DM血清IL-6和脂联素的变化

选择无任何并发症血糖控制不佳的T2DM患者30例，于胰岛素联合罗格列酮治疗，并与30例正常对照组比较。结果：①T2DM组血清IL-6水平显著高于血清脂联素水平显著低于正常对照组（P〈0．05）。②治疗后较治疗前IL-6水平显著降低，脂联素水平显著升高（P〈0．05）。结论：罗格列酮通过降低IL-6水平和增加脂联素水平减轻胰岛素抵抗和保护胰岛β细胞的功能。     

高血压患者血清脂联素水平和动脉顺应性的关系

目的探讨高血压人群中血清脂联素浓度和动脉顺应性之间的关系。方法入选非糖尿病的高血压受试者83例,分为药物治疗组和未治疗组。常规检测受试者的坐位血压及部分血清生化指标,包括血糖、血脂、肝功能、肾功能和胰岛素水平;放射免疫法检测血清脂联素浓度;计算稳态模式胰岛素抵抗指数(HOMA-IR);用HDICVprofilor DO-2020检测大动脉弹性指数(C1)和小动脉弹性指数(C2)。结果比较药物治疗组和未治疗组,发现前者的脂联素浓度(中位数:11.9μg/mL)、C1(中位数:13.7mL/mmHg×10)、C2(中位数:4.3mL/mmHg×100)均明显高于后者(5.7μg/mL,10.7mL/mmHg×10,3.7mL/mmHg×100,P均<0.01)。对未治疗组进行相关分析发现LogC1与脂联素浓度明显正相关(r=0.54,P<0.01),与平均血压(MBP)负相关(r=-0.40,P<0.05);LogC2和脂联素浓度明显正相关(r=0.49,P<0.01),与HOMA-IR和MBP明显负相关(LogC2-HOMA-IRr=-0.40,P<0.05;LogC2-MBP,r=-0.32,P<0.01);另外还发现C1与心率(HR)负相关(LogC1-HRr=-0.41,P<0.01)。多元线性逐步回归分析发现血清脂联素浓度和HR水平以及性别是LogC1的独立影响因素(R2=0.39,P<0.01);血清脂联素水平和性别是LogC2的独立影响因素(R2=0.44,P<0.01)。结论高血压人群中C1,C2的减退与血清脂联素浓度的降低密切相关。接受抗高血压药物治疗的患者,血清脂联素浓度和动脉顺应性水平升高。     

原发性高血压患者血清脂联素水平与IL-6的相关性

目的:探讨高血压患者血清脂联素(adiponectin,APN)水平,以及APN与白细胞介素-6(interlectin-6,IL-6)的相关性。方法: 选取原发性高血压患者60例(HT组,其中高血压Ⅰ级、Ⅱ级和Ⅲ级患者分别为20例),健康对照者20例(Control组),采用酶联免疫吸附法测定两组患者血清APN水平和IL-6水平。结果: 高血压患者血清APN水平［(8.2±3.8) mg/L］显著低于健康对照组［(10.4±2.9) mg/L］(P<0.05),而IL-6水平［(81±4) μg/L］高于健康对照组［(18±5) μg/L］(P<0.05),APN水平与IL-6呈负相关(r=-0.782,P<0.05)。多元回归分析表明,收缩压、高血压分级和IL-6水平可显著影响原发性高血压患者血清APN水平的变化。结论: 原发性高血压患者存在低脂联素血症,且与高血压严重程度密切相关。     

老年高血压和代谢综合征血清脂联素水平变化及其意义

目的:探讨老年高血压和代谢综合症患者血清脂联素水平变化及其意义。方法:60例老年高血压患者、62例老年代谢综合症患者和30例正常老年对照者,检测血压、体重、身高、腰围、空腹血糖、胰岛素、游离脂肪酸、血清脂联素、高敏C反应蛋白、尿素氮、肌酐,计算体重指数,测尿微量蛋白。结果:(1)高血压组和代谢综合症组脂联素水平明显低于正常对照组(P<0.05),体重指数、腹围、尿微量蛋白、游离脂肪酸、血糖、胰岛素、肌酐水平均高于对照组(P<0.05);(2)直线相关分析表明,血清脂联素水平与血压、尿微量蛋白、体重指数、腰围均成负相关(r=-0.230~-0.304,P<0.05~<0.01)。结论:代谢综合症和单纯高血压老年患者脂联素水平降低,且脂联素水平与血压、BMI、腰围及尿微量蛋白呈负相关。     

尿脂联素与糖尿病肾病严重程度的相关性研究

目的 探讨尿脂联素与糖尿病肾病严重程度的相关性.方法 150例糖尿病患者根据尿微量白蛋白/肌酐(ACR)分为正常白蛋白尿组(ACR＜ 30 mg/g),微量白蛋白尿组(ACR30～300 mg/g),大量白蛋白尿组(ACR＞ 300 mg/g),每组均为50例.同时选取健康体检者30名作为对照组.应用全自动生化分析仪测定空腹血糖、HbA1c、肌酐、白蛋白、甘油三酯、总胆固醇、高密度脂蛋白-胆固醇(HDL-C)、低密度脂蛋白-胆固醇(LDH-C)等生化指标.采用酶联免疫吸附法测定血、尿脂联素水平.结果 血、尿脂联素及HbA1c水平在对照组、正常白蛋白尿组、微量白蛋白尿组及大量白蛋白尿组中依次升高,差异均有统计学意义(F=62.46,65.26,5.37,P均＜0.05);血肌酐水平随尿白蛋白水平升高依次升高,微量白蛋白尿组及大量白蛋白尿组与对照组之间比较,差异有统计学意义(F=8.25,P＜0.05),微量白蛋白尿组及大量白蛋白尿组与正常白蛋白尿组之间比较无明显统计学意义(P＞0.05);估算的肾小球滤过率(eGFR)随尿白蛋白水平升高依次降低(F=54.67,P＜0.01).Pearson相关分析显示尿脂联素与血肌酐、ACR、血脂联素、HbA1c呈正相关(r=0.66,0.61,0.62,0.35,P均＜0.05),与eGFR呈负相关(r=-0.71,P＜0.01).多元逐步回归分析发现尿脂联素与血肌酐、HbA1c、ACR、eGFR及血脂联素相关(P均＜0.05).结论 尿脂联素与糖尿病肾病的严重程度呈正相关.     

Interleukin 6, adiponectin, leptin, and insulin resistance in nonobese Japanese type 2 diabetic patients

The aim of the present study was to investigate the relationships between interleukin 6 (IL-6) and insulin resistance, serum leptin, serum adiponectin, or serum lipids including triglycerides in 98 nonobese Japanese type 2 diabetic patients. Insulin resistance was estimated by the insulin resistance index of homeostasis model assessment (HOMA-IR). Serum IL-6 concentration was negatively correlated to high-density lipoprotein cholesterol (r = -0.295, P = .004), but was not associated with HOMA-IR (r = 0.016, P = .871), body mass index (BMI) (r = 0.090, P = .375), systolic (r = 0.169, P = .116) and diastolic (r = -0.061, P = .570) blood pressures, leptin (r = 0.062, P = .544), and adiponectin (r = -0.020, P = .841) in these patients. In contrast, serum leptin level was positively correlated to HOMA-IR (r = 0.291, P = .004), BMI (r = 0.338, P < .001), and systolic blood pressure (r = 0.241, P = .025). Serum adiponectin level was negatively correlated to HOMA-IR (r = -0.288, P = .005), BMI (r = -0.308, P = .002), diastolic blood pressure (r = -0.269, P = .012), and triglycerides (r = -0.338, P < .001), and positively correlated to high-density lipoprotein cholesterol (r = 0.300, P = .003) in our patients. From these results, it can be suggested that fasting serum IL-6 is not a major factor responsible for the evolution of insulin resistance in nonobese Japanese type 2 diabetic patients.     

Hypoadiponectinemia is associated with blood pressure increase in obese insulin-resistant individuals

Adiponectin is a major adipocytokine and has been considered as an independent risk factor for arterial hypertension. Most studies on the subject have been restricted to biracial (white-black) and Asian groups. The present report examined whether adiponectin affects blood pressure in a sample of untreated obese Brazilians of multiethnic origin. Fasting plasma adiponectin and serum insulin were determined by radioimmunoassay. Insulin resistance was estimated by homeostatic model assessment of insulin resistance (HOMA-IR). Blood pressure was recorded using Dinamap 1846 (Critikon, Tampa, FL). Adiponectin was significantly lower in obese hypertensive individuals than in obese normotensive ones. Blood pressure, insulin, and HOMA-IR were significantly higher in obese hypertensive than in obese normotensive individuals. Plasma adiponectin was negatively associated with waist-to-hip ratio, blood pressure, insulin, and HOMA-IR. The comparison of obese individuals who markedly differed in their HOMA-IR (> vs 6. 5 microg/mL), a 3 x 2 analysis of variance showed an independent contribution of adiponectin in the variation of mean arterial pressure. These results support the notion that HOMA-IR and adiponectin independently predict blood pressure variation in obese insulin-resistant Brazilians.     

The negative correlation between plasma adiponectin and blood pressure depends on obesity: a family-based association study in SAPPHIRe

BACKGROUND: The association between plasma adiponectin level and blood pressure remains inconclusive. Because obese subjects may have different mechanisms to regulate blood pressure, we hypothesized that obesity may be an important modifier. In order to minimize confounding effects from unidentified factors, a family-based design was employed to explore the relationship. METHODS: A total of 1,048 subjects from 478 Chinese or Japanese families with a mean age of 50.4 +/- 9.0 years were included (the SAPPHIRe (Stanford-Asian Pacific Program in Hypertension and Insulin Resistance) cohort). Blood pressure was recorded automatically and the average of the last two out of three consecutive readings was used in the analysis. A subject with "hypertension" was defined as one with a systolic blood pressure (SBP) > or =140 mm Hg, or a diastolic blood pressure (DBP) > or =90 mm Hg, or who was already on medication for hypertension. Obesity was defined as having a body mass index (BMI) > or =25 kg/m(2). The updated homeostasis model assessment was used for calculating the indices of insulin sensitivity (HOMA2 %S). Fasting plasma adiponectin was determined using radioimmunoassay. RESULTS: Subjects with hypertension had significantly lower plasma adiponectin levels than those without hypertension (5.99 +/- 3.64 microg/ml vs. 6.65 +/- 3.86 microg/ml, P < 0.01). Plasma adiponectin level correlated negatively with hypertension after adjusting for age, sex, and HOMA2%S (odds ratio (OR) 0.94, 95% confidence interval (CI) 0.90-0.98). In subjects without hypertension (n = 349), the plasma adiponectin level correlated negatively with SBP in those who were obese, after adjustment for age, sex, BMI, and HOMA2 %S (beta = -0.58, P = 0.03). The association was not significant in those without obesity. CONCLUSIONS: Plasma adiponectin level correlates negatively with hypertension. In subjects without hypertension, the relationship between plasma adiponectin level and SBP depends on the presence of obesity.     

Relationship of adiponectin to serum paraoxonase 1

Correlation of the plasma levels of insulin-sensitizing, anti-inflammatory and anti-atherosclerotic adiponectin with HDL has been demonstrated. However, its relation to HDL-bound paraoxonase 1 (PON1) has not been clarified. The association of serum PON1 activity with findings of metabolic syndrome was investigated in three age and sex-matched groups: (1) non-diabetic overweight subjects with BMI 28-39.9 kg/m(2) (n=25); (2) non-diabetic obese subjects with BMI>or=40 kg/m(2) (n=25); and (3) healthy, normal-weight controls (n=24). Of the parameters investigated, PON1 activity correlated positively with concentrations of HDL-C and adiponectin, and correlated negatively with BMI, waist circumference, systolic BP, levels of HbA(1C), and insulin, HOMA-IR, and TBARS. The positive correlation between adiponectin and PON1 remained significant even after adjustments for age, gender, BMI, blood pressure, HOMA-IR, HDL-C, LDL-C, and lipid peroxidation. CONCLUSIONS: PON1 activity shows negative association with markers of metabolic syndrome. We demonstrate that adiponectin is an independent variable of serum PON1, which may contribute to the anti-atherosclerotic effect of adiponectin.     

Insulin resistance, adipokines, and oxidative stress in nondiabetic, hypercholesterolemic patients: leptin as an 8-epi-prostaglandin F2alpha determinant

Limited data are available on the association of insulin resistance, adipokines, and in vivo lipid peroxidation. We investigated the relationships between insulin resistance, adipokines (leptin, adiponectin, and resistin), and oxidative stress in nondiabetic, hypercholesterolemic patients. Seventy-six nondiabetic patients with hypercholesterolemia participated in this cross-sectional study. Fasting glucose and insulin concentrations were analyzed. Serum leptin, adiponectin, and resistin concentrations and urinary excretion of 8-epi-prostaglandin F(2alpha) (8-epi-PGF(2alpha)) were determined using enzyme-linked immunosorbent assay. We divided all subjects into 3 groups, classified by the tertiles of homeostasis model assessment of insulin resistance (HOMA-IR) values, and clinical parameter comparisons were made among the 3 groups. The results showed that serum leptin (P < .001) and adiponectin levels (P < .05) were significantly different among the groups, although serum resistin was not different. Furthermore, the group with the highest HOMA-IR had a significantly higher urinary 8-epi-PGF(2alpha) excretion than the group with the lowest HOMA-IR (P = .017). Circulating leptin was positively correlated with urinary 8-epi-PGF(2alpha) (r = 0.323, P < .01) and HOMA-IR (r = 0.524, P < .001). Circulating adiponectin was negatively correlated with body mass index (r = -0.252, P < .05) and HOMA-IR (r = -0.228, P < .05). We could not find a relationship between circulating adiponectin or resistin and urinary 8-epi-PGF(2alpha) excretion. Stepwise multiple linear regression analysis showed that leptin was associated with the urinary 8-epi-PGF(2alpha) excretion after adjusting for age, sex, body mass index, blood lipids, and HOMA-IR (P = .002). In conclusion, our results show that more insulin-resistant state of nondiabetic, hypercholesterolemic patients is associated with decreased adiponectin and increased leptin and urinary 8-epi-PGF(2alpha) levels, although no relationship with resistin was observed. Furthermore, serum leptin independently contributed to urinary 8-epi-PGF(2alpha) excretion.