2型糖尿病合并肥胖患者脂联素水平与胰岛素抵抗的相关性

目的 研究2型糖尿病合并肥胖患者脂联素水平和胰岛素抵抗之间的相关性,探讨脂联素在2型糖尿病合并肥胖患者发生胰岛素抵抗中的作用.方法 选择30例2型糖尿病合并肥胖患者、25例2型糖尿病患者及25例非糖尿病对照人员(其中13例为肥胖者),检测体质指数、腰/臀比值、空腹血糖、糖化血红蛋白、血清空腹胰岛素、血脂、脂联素水平,计算胰岛素抵抗指数和胰岛素敏感指数.分析血清脂联素与胰岛素抵抗的相关性.结果 (1)糖尿病肥胖组的检测体质指数、糖化血红蛋白、空腹血糖、胰岛素抵抗指数、血清空腹胰岛素、腰/臀比值均高于对照肥胖组,脂联素、胰岛素敏感指数低于对照肥胖组(P<0.05).(2)糖尿病非肥胖组甘油三酯、糖化血红蛋白、空腹血糖、胰岛素抵抗指数、血清空腹胰岛素均高于对照非肥胖组,胰岛素敏感指数、脂联素低于对照非肥胖组(P<0.05).(3)糖尿病肥胖组甘油三酯、胆固醇、体质指数、糖化血红蛋白、空腹血糖、胰岛素抵抗指数、血清空腹胰岛素、腰/臀比值均高于糖尿病非肥胖组,胰岛素敏感指数、脂联素低于糖尿病非肥胖组(P<0.05).结论 脂联素与2型糖尿病肥胖患者的胰岛素抵抗发生有关,脂联素降低易导致胰岛素抵抗,脂联素水平可作为2型糖尿病合并肥胖患者发生胰岛素抵抗的监测标准.     

非酒精性脂肪肝血浆抵抗素与肥胖和胰岛素抵抗关系的研究

目的探讨非酒精性脂肪肝(NAFLD)血浆抵抗素与肥胖和胰岛素抵抗的关系。方法对兰州大学第一医院2005年10月至2006年2月60例NAFLD患者和28名年龄、性别相匹配的正常对照者,采用ELISA方法测定空腹血浆抵抗素,同时检测其身高、体重、腰围、臀围、血压、血糖、血脂、肝功能及胰岛素水平,并计算体重指数、脂肪百分比、腰臀比和胰岛素抵抗指数。结果NAFLD组与正常对照组相比,其血浆抵抗素明显升高[(8.56±2.5)ng/mL对(6.39±2.81)ng/mL,P<0.01]。相关分析显示血浆抵抗素与空腹胰岛素、胰岛素抵抗指数呈显著正相关(分别为r=0.271,P=0.036;r=0.30,P=0.020);而与腰臀比、体重指数、脂肪百分比、收缩压、舒张压、总胆固醇、甘油三酯、低密度脂蛋白胆固醇、高密度脂蛋白胆固醇、血糖无相关性(P>0.05)。结论NAFLD患者血浆抵抗素明显升高,与胰岛素抵抗程度呈显著正相关,与肥胖无相关性。因而抵抗素可能主要与肝源性胰岛素抵抗有关,而与肥胖相关的胰岛素抵抗无关。     

非酒精性脂肪肝患者血清抵抗素与胰岛素抵抗关系的研究

目的 探讨非酒精性脂肪肝患者血清抵抗素水平及其与肥胖、胰岛素抵抗、血糖、血脂的关系.方法 选择非酒精性脂肪肝患者100例,正常对照30例,采用ELISA方法测定空腹血清抵抗素,同时检测其身高、体重、腰围、臀嗣、血糖、血脂、肝功能及胰岛素水平,并计算体重指数、腰臀比和胰岛索敏感指数.结果 非酒精性脂肪肝患者血清抵抗素水平为17.68±5.2 ng.ml,高于正常对照组的12.85±4.4 ng.ml,P<0.01.相关分析显示,血清抵抗素与体重指数、甘油三酯呈正相关关系(分别为r=0.376、0.426,P<0.05),与胰岛素敏感指数呈负相关关系,(r=-0.584,P<0.01),而与腰臀比、总胆固醇、低密度酯蛋白胆固醇、高密度脂蛋白胆固醇、血糖无相关性,(P>0.05).结论 在非酒精性脂肪肝的发病过程中,抵抗素可能参与了胰岛素抵抗.     

血浆脂联素与2型糖尿病胰岛素抵抗关系的研究

目的　测定 2型糖尿病患者血浆脂联素的水平 ,并分析它与体重指数、血糖、胰岛素、血脂和胰岛素抵抗的关系 ,从而探讨脂联素在糖尿病发病中的作用。方法　健康对照组 2 8例 ,2型糖尿病组 60例 ,根据体重指数又将糖尿病组分为非肥胖糖尿病组 3 0例 (BMI <2 5kg/m2 )和肥胖糖尿病组 3 0例 (BMI >2 5kg/m2 )。用ELISA方法检测空腹血浆脂联素浓度 ,同时测定各组的空腹血糖、胰岛素、血脂的水平 ;根据HOMA模型提出的公式 ,计算分析胰岛素抵抗指数 ,并分析各指标间的相关性。结果　 (1)糖尿病各组血浆脂联素的水平明显低于正常对照组 ,且肥胖糖尿病组脂联素的水平低于非肥胖组 ,差异均有显著性 (P 0 .0 1) ;(2 )血浆脂联素浓度与体重指数、空腹胰岛素、胰岛素抵抗指数 (IR)、甘油三酯呈显著负相关。结论　脂联素参与了胰岛素抵抗的发生过程 ,与糖尿病的发生发展密切相关 ;脂联素可作为评价胰岛素抵抗程度的一种新的敏感指标     

肥胖的2型糖尿病人血浆C反应蛋白水平与胰岛素抵抗的关系

目的　了解肥胖的 2型糖尿病患者血浆C反应蛋白 (CRP)水平及其与胰岛素敏感性的关系。方法　受试者分为 3组 :肥胖的 2型糖尿病组 ( 4 2例 )、非肥胖的 2型糖尿病组组 ( 4 0例 )和正常体重对照组 ( 3 7例 )。空腹静脉取血 ,测定血浆中CRP、血脂 (TG和TC) ,空腹血糖 (FPG )和空腹血浆胰岛素 (FPI) ,并计算胰岛素敏感性指数 (ISI)。结果　血浆CRP水平在肥胖组 ( 89.0 1±10 .87mg/L)明显高于非肥胖组 ( 5 4.45± 9.83mg/L) (P <0 .0 5 )和正常体重对照组( 3 9.40± 8.2 9mg/L) (P <0 .0 1) ;非肥胖组与对照组之间比较无显著差异 (P >0 .0 5 )。血浆CRP水平与ISI呈显著负相关 (r =-0 .42 ,P <0 .0 1) ;与空腹甘油三酯水平呈正相关 (r =0 .3 5 ,P <0 .0 5 )。结论　肥胖的 2型糖尿病组患者血浆CRP水平上升可能与胰岛素抵抗有关     

2型糖尿病患者血浆脂联素和抵抗素水平的测定及意义

为探讨2型糖尿病患者血浆脂联素和抵抗素水平的变化及意义。将60例2型糖尿病患者分为非肥胖糖尿病组30例(体质指数<25kg/m2)和肥胖糖尿病组30例(体质指数>25kg/m2);并选择28例健康者作对照。用酶联免疫吸附检测法测空腹血浆脂联素和抵抗素浓度;并测定各组的空腹血糖、胰岛素和血脂的水平;根据HOMA稳态模型提出的公式,计算胰岛素抵抗指数和胰岛素敏感指数,分析各指标间的相关性。结果发现,①糖尿病各组血浆脂联素的水平明显低于对照组,且肥胖糖尿病组低于非肥胖组,差异有显著性(P<0.01)。②糖尿病各组血浆抵抗素的水平明显高于对照组,而且肥胖糖尿病组明显高于非肥胖组,差异有显著性(P<0.01)。③相关分析发现,血浆脂联素浓度与体质指数、空腹血糖、胰岛素抵抗指数和甘油三酯呈显著负相关(分别为r=-0.55,P<0.01;r=-0.51,P<0.01;r=-0.52,P<0.01;r=-0.39,P<0.05),而与胰岛素敏感指数呈显著正相关(r=0.45,P<0.01);抵抗素则与体质指数、空腹血糖、胰岛素抵抗指数和甘油三酯呈显著正相关(r=0.40,P<0.01;r=0.52,P<0.01;r=0.46,P<0.01;r=0.27,P<0.05);与胰岛素敏感指数)呈显著负相关(r=-0.32,P<0.01)。此结果提示,脂联素和抵抗素都参与了胰岛素抵抗的发生过程,可能与2型糖尿病的糖脂代谢紊乱有关。     

2型糖尿病患者血浆Apelin-12水平与高血压、胰岛素抵抗的相关性

目的探讨Apelin-12与高血压、肥胖、胰岛素抵抗、炎症等的相关性。方法测定31例单纯2型糖尿病、37例2型糖尿病合并高血压患者及25例健康对照者血浆Apelin-12、肿瘤坏死因子α(TNF-α)、血脂、糖化血红蛋白(HbA1c)、空腹血糖、空腹胰岛素(FINS)、胰岛素抵抗(IR)指数(HOMA-IR)、体重指数(BMI)、血压等水平并进行各参数之间的相关分析。结果①糖尿病合并高血压组血浆Apelin-12水平低于正常对照组和单纯糖尿病组(P0.05或P0.01),单纯糖尿病组血浆Apelin-12水平高于正常对照组(P0.05)。②糖尿病合并高血压组TNF-α水平高于糖尿病组和正常对照组(P0.05或P0.01),糖尿病组TNF-α水平高于正常对照组(P0.05)③直线相关分析显示,空腹血浆Apelin-12与腰臀比(WHR),FINS,HOMA-IR,甘油三酯(TG),收缩压(SBP),TNF-α呈负相关,与HDL-C呈正相关。结论血浆Apelin-12水平在糖尿病组升高,在糖尿病合并高血压组降低,且与肥胖、IR、炎症等相关。推测Apelin-12可能参与了IR、2型糖尿病、高血压等疾病的发生发展。     

妊娠期糖尿病患者血浆抵抗素水平与胰岛素抵抗的关系

采用ELISA方法检测正常妊娠妇女(对照组)及妊娠期糖尿病(GDM)患者(GDM组)的空腹血浆抵抗素浓度,并测定空腹血糖(FPG)、空腹胰岛素(FIN)及血脂,计算体质量指数(BMI)及胰岛素抵抗指数(HOMA-IR);分析抵抗素与FPG、FIN、血脂、HOMA-IR的相关性.结果 :①DGDM组血浆抵抗素、BMI、FIG、FIN、总胆固醇、甘油三酯及HOMA-IR均明显高于对照组(P均＜0.05);②GDM组血浆抵抗素浓度与BMI、FPG、甘油三酯、HOMA-IR呈显著正相关(r=0.47、0.49、0.42、0.62,P均＜0.05).认为抵抗素参与了GDM胰岛素抵抗的发生;血浆抵抗素浓度可能作为评价GDM胰岛素抵抗程度的一种新的敏感指标.     

2型糖尿病患者大网膜与皮下脂肪组织抵抗素蛋白表达的研究

目的了解2型糖尿病(T2DM)患者大网膜与皮下脂肪组织抵抗素蛋白表达的情况,探讨肥胖和糖尿病间的关系.方法 Western blot 法检测大网膜及皮下脂肪组织抵抗素表达情况;测定空腹血胰岛素水平和血糖浓度,并计算胰岛素敏感指数;测量身高、体重、腰围、臀围、收缩压、舒张压,计算腰臀比、体重指数、体内脂肪百分比.结果以OD值表示,正常对照组(57411±1225.59)大网膜与皮下脂肪组织抵抗素蛋白表达明显较单纯肥胖组(41671±884.38,P<0.01)、非肥胖T2DM组(42131±1286.15,P<0.01)、肥胖T2DM组(42677±1751.10,P<0.05)表达增高,后三组抵抗素蛋白表达无明显差异.四组自身的大网膜与皮下脂肪组织抵抗素蛋白表达无显著差异.逐步回归分析示腰臀比、体重指数、空腹血糖对抵抗素表达的作用显著.结论正常对照组大网膜与皮下脂肪组织抵抗素蛋白表达明显较单纯肥胖组、非肥胖T2DM组、肥胖T2DM组表达增高,抵抗素与腰臀比、体重指数、空腹血糖呈显著负相关提示人体抵抗素可能不是肥胖和糖尿病的联系所在.     

内脂素与肥胖和糖代谢异常的关系

目的 探讨内脂素与肥胖和糖代谢异常的关系.方法 根据受检者的血糖、病程和肥胖程度分为正常糖耐量(NGT组)、糖调节受损(IGR组)、初诊2型糖尿病(T2DM,A组)、已诊T2DM(B组)、肥胖组和非肥胖组,用ELISA法测定各组空腹血浆内脂素,分析其与体质量指数、腰围(WC)、腰臀比、血糖、血脂、血压、真胰岛素、胰岛素抵抗指数和胰岛β细胞功能指数等关系.结果 A、B组内脂素水平明显高于NGT组(P<0.05,<0.01),B组高于A组(P<0.05),肥胖组高于非肥胖组(P<0.01).内脂素水平与糖化血红蛋白、WC呈独立正相关,与糖负荷后2h胰岛素呈独立负相关.结论 血浆内脂素与肥胖和糖代谢状态有关,可能在T2DM发病中起重要作用.     

2型糖尿病血浆抵抗素水平与胰岛素敏感性相关因素的研究

2型糖尿病患者血浆抵抗素水平明显高于正常人；在糖尿病患者中血浆抵抗素水平肥胖者明显高于非肥胖者，且与胰岛素敏感指数（ISI）呈负相关，与FPG、血脂、年龄、性别，WHR无相关性。     

老年高血压患者血浆抵抗素水平与胰岛素抵抗的相关性

目的了解老年高血压患者血浆抵抗素水平与胰岛素抵抗的关系。方法选择41例中青年人(对照组)和43例老年人(老年组),分别分为高血压组和正常血压组,用竞争性酶联免疫吸附试验测定各组空腹血浆抵抗素水平,同时测定空腹血糖、空腹胰岛素、血脂和胰岛素敏感指数,测量受试对象腰围、臀围和腰臀比。结果老年组血浆抵抗素水平与对照组相比明显升高(P<0.05),老年组中高血压亚组血浆抵抗素与正常血压亚组相比差异无显著性。对照组高血压亚组抵抗素水平略高于正常血压亚组,但差异无统计学意义(P>0.05)。抵抗素与年龄呈正相关(r=0.31,P<0.01;r=0.28,P<0.05),与体质指数呈正相关(r=0.23,P<0.05),与胰岛素抵抗指数呈负相关(r=-0.31,P<0.05),但在各实验组中,抵抗素与体质指数无明显相关性。结论空腹血浆抵抗素水平与年龄和体质指数呈正相关,与胰岛素抵抗指数呈负相关。     

抵抗素与肥胖及2型糖尿病的关系

目的探讨抵抗素与肥胖及2型糖尿病(T2DM)的相关性。方法正常人(NC)80例、单纯肥胖(Ob)67例、T2DM77例、伴肥胖的T2DM(Ob DM)102例,测定其血清抵抗素、真胰岛素、胰岛素原、胰升糖素、空腹血糖、血脂及血压等水平,记录身高、体重等。结果四组抵抗素水平差异无统计学意义(P>0.05);抵抗素与胰岛β细胞功能、胰岛素敏感性也无相关性(P>0.05);在Ob、DM及Ob DM组抵抗素与TC呈正相关(r=0.35,0.33,0.38,P<0.05);在Ob及Ob DM组抵抗素与腰臀比呈正相关(r=0.36,0.27,P<0.05);在Ob组抵抗素与PI呈正相关(r=0.37,P<0.05)。结论抵抗素与T2DM无相关性,但可能影响肥胖及糖尿病患者的脂质代谢及胰岛素抵抗的形成。     

血清抵抗素水平与肥胖及胰岛素抵抗相关性的研究

目的　探讨 2型糖尿病 (T2DM)患者血清抵抗素水平与肥胖及胰岛素抵抗 (IR)的关系。方法　酶联免疫法测定T2DM患者 86例及对照组 42例的空腹血清抵抗素水平。记录受试对象性别、年龄、病程、身高、体重、腰围 (W )、臀围 (H)、血压 ,并检测空腹血脂、血糖 (Glu)、肾功能、胰岛素 (INS)、雌二醇 (E2 )、睾酮 (T)等生化指标。结果　无论是T2DM组还是对照组 ,肥胖者血清抵抗素水平与非肥胖者比较 ,均具有统计学差异(P <0 0 1 ) ,T2DM组与对照组比较其血清抵抗素水平无显著性差异 ;采用相关分析发现 ,血清抵抗素浓度与BMI、腰围、WHR、BF %、TG、ApoB、FINS、SBP、DBP呈显著正相关 ,与ISI显著负相关 ,男性抵抗素水平与T呈正相关 ;采用多元逐步回归分发现BF %、FINS、ISI、腰围为影响抵抗素最显著的因素 (R2 =0 78)。结论　T2DM组与对照组比较其血清抵抗素水平无显著性差异 ,而无论是T2DM组还是对照组 ,肥胖者血清抵抗素水平与非肥胖者比较 ,差别均具有统计学意义 (P <0 0 0 1 )。血清高抵抗素水平与BF %、FINS、ISI、腰围的相关性提示 ,抵抗素可能在肥胖、IR及T2DM的发病中起一定作用     

超重及肥胖人群血清网膜素-1水平的变化

目的 探讨在南京地区人群中超重及肥胖者血清网膜素-1水平的变化及其与体重指数、腰围、脂联素之间的相关性.方法 从2008年3月至7月全国糖尿病和代谢综合征患病率及变迁调查江苏分中心的南京地区调查人群中,选取42例超重及肥胖者和55名健康对照者,分别测定体重指数、腰围、空腹胰岛素、窄腹血糖、血脂、血清网膜素-1及脂联素的水平,计算腰臀比及胰岛素抵抗指数.采用SPSS 15.0软件进行统计学分析,血清网膜素-1和各指标问的相关性分析采用Pearson相关分析法.结果 健康对照者的血清网膜素-1浓度为(0.024±0.012)μg/L,脂联素浓度为(7.7±2.4)mg/L,超重及肥胖者的血清网膜素-1浓度为(0.016±0.007)μg/L,脂联素浓度为(6.4±3.1)mg/L.结果 显示超重及肥胖者的血清网膜素-1及脂联素水平明显低于健康对照者(P<0.05),且相关分析表明血清网膜素-1与体重指数(r=-0.321,P<0.05)、腰围(r=-0.312,P<0.05)、腰臀比(r=0.243,P<0.05)及甘油三脂(r=-0.220,P<0.05)之间旱显著负相关,与脂联索(r=0.232,P<0.05)呈明显正相关.结论 超莆及肥胖者的血清网膜素-1水平较健康对照者显著下降,且血清网膜素-1浓度变化与脂联素之间呈正相关,提示网膜素水平变化可能与肥胖、胰岛素抵抗和2型糖尿病密切相关.     

Plasma resistin, adiponectin and leptin levels in lean and obese subjects: correlations with insulin resistance

OBJECTIVE: Adipose tIssue regulates insulin sensitivity via the circulating adipocytokines, leptin, resistin and adiponectin. The objective of this study was to compare the levels of resistin, adiponectin and leptin in lean and obese subjects and determine the relationship between circulating adipocytokines and insulin resistance. METHODS: We examined plasma levels of resistin, adiponectin and leptin in 17 lean subjects with a mean body mass index (BMI) of approximately 23 and 34 non-diabetic obese individuals with a mean BMI approximately 33. Insulin resistance was assessed using the homeostasis model assessment ratio (HOMA-R) formula derived from fasting insulin and glucose levels. RESULTS: Resistin levels were not significantly different between the two groups but were significantly higher in women compared with men, 35.4+/-6.5 (s.e.) vs 15.4+/-2.9 microg/L, P<0.01. Resistin did not correlate with BMI but did significantly correlate with HOMA-R, P<0.01, and this correlation remained significant after adjustment for gender and BMI. Adiponectin levels were significantly lower in obese compared with lean subjects, P<0.005, and higher in women, P<0.001, but showed no significant correlation with HOMA-R. Leptin levels were significantly higher in obese subjects and women and correlated with HOMA-R and resistin. DISCUSSION: In this small group of patients we demonstrated that insulin resistance correlated most strongly with leptin levels. A significant correlation between resistin levels and insulin resistance was also observed. Although a similar trend was apparent for adiponectin, the correlation with insulin resistance did not achieve statistical significance.     

Increased serum resistin in nonalcoholic fatty liver disease is related to liver disease severity and not to insulin resistance

CONTEXT: The recently discovered hormone resistin is linked to the development of insulin resistance, but direct evidence of resistin levels in humans with nonalcoholic fatty liver disease (NAFLD) is lacking. METHODS: We conducted this study to assess the relationship between serum resistin and NAFLD. We measured serum resistin and biochemical, hormonal, and histological correlates in 28 NAFLD patients, 33 controls, and 30 obese patients [body mass index (BMI), >30 kg/m2] without NAFLD. RESULTS: Resistin and adiponectin expression were measured in sc adipose tissue by quantitative RT-PCR. Resistin was higher in NAFLD patients compared with controls (5.87 +/- 0.49 vs. 4.30 +/- 0.20 ng/ml; P = 0.002) and obese patients (4.37 +/- 0.27 ng/ml; P = 0.002). Increased resistin mRNA was also found in the adipose tissue of NAFLD patients compared with controls and obese subjects. CONCLUSIONS: Both NAFLD and obese patients had lower adiponectin levels, whereas leptin was increased only in the obese group. No correlation was found between resistin and high-sensitivity C-reactive protein, BMI, homeostasis model assessment, insulin, glucose, transaminases, and lipid values. A positive correlation was found between resistin and histological inflammatory score. These data report increased resistin in NAFLD patients that is related to the histological severity of the disease, but do not support a link between resistin and insulin resistance or BMI in these patients.     

胰岛素治疗对血浆抵抗素水平的影响

经ELISA方法测得的空腹血浆抵抗素水平，2型糖尿病患者显著高于正常对照组（P〈0．05）；而在有和无糖尿病微血管病患者之间，不存在明显差异（P〉0．05）。经胰岛素治疗，血抵抗素水平明显下降。     

Plasma insulin, cholecystokinin, galanin, neuropeptide Y and leptin levels in obese women with and without type 2 diabetes mellitus

Obesity is an important factor predisposing to type 2 diabetes mellitus, especially for postmenopausal women. Experimental studies provided evidences that leptin, cholecystokinin (CCK), galanin (GAL), neuropeptide Y (NPY) and insulin are involved in feeding behaviour. The aim of the study was to evaluate their possible relationships in obese and diabetic women. Three groups of postmenopausal women (FSH > 30 mIU/ml) were evaluated: 8 diabetic (mean age 56.6 +/- 6.9 y, BMI 29.8 +/- 5.3 kg/m2), 10 obese non-diabetic (mean age 49.6 +/- 5.4 y, BMI 36.0 +/- 3.7 kg/m2) and 12 non-diabetic controls (mean age 52.7 +/- 3.5 y, BMI 27.3 1.9 kg/m2). For each patient BMI and WHR were measured and calculated. Blood samples were collected at 8:00 a.m. after an overnight fast. Plasma concentrations of FSH, leptin, CCK, GAL, NPY and insulin were determined using commercial RIA kits. Mean plasma NPY concentration was significantly higher in diabetic women than in controls (190.1 pg/ml +/- 85.4 vs 120.4 +/- 36.6). Compared to controls, mean plasma leptin level was significantly higher in obese non-diabetic women (32.9ng/ml +/- 9.2 vs 18.9 +/- 9.1). No significant differences were found between obese non-diabetic and diabetic women. In diabetic subjects positive correlations were found between: CCK and leptin (r= 0.8295; P= 0.011), CCK and insulin (r=0.7832; P=0.022), leptin and insulin (r=0.9302; P=0.001). In obese subjects a positive correlation between WHR and GAL (r= 0.6624; P= 0.037) and a negative between GAL and insulin (r= -0.6795; P= 0.031) were found. In controls positive correlations were found between WHR and CCK (r=0.6412; P=0.025), GAL and insulin (r=0.630; P=0.028) and negative between CCK and NPY (r = -0.6505; P= 0.022). Our results, ie higher mean plasma NPY levels in postmenopausal diabetic women and positive correlation of CCK with leptin and insulin, may suggest the role of these neuropeptides in metabolic disorders leading to type 2 diabetes mellitus.     

Serum resistin level among healthy subjects: relationship to anthropometric and metabolic parameters

Resistin is a novel adipocyte-secreted hormone that has been proposed to be the link between obesity and diabetes, although little appears to be known regarding the physiological role of resistin in human beings. We aimed to explore the relationship between serum resistin level and certain anthropometric and metabolic parameters. Seventy-one healthy subjects with a mean body mass index of 23 kg/m 2 or greater were recruited in this study. Anthropometric measurements including height, weight, body mass index, waist and hip circumferences, waist-to-hip ratio, and blood pressure were recorded. Insulin resistance was measured by homeostasis model assessment (HOMA). Fasting serum resistin, insulin and plasma glucose, lipid profiles, and uric acid levels were measured. The results revealed that serum resistin level did not correlate with any markers for adiposity, blood pressure, fasting plasma glucose, or uric acid level for either sex. Serum resistin level correlated negatively with fasting insulin level (gamma=-0.455, P=.006) and HOMA (gamma=-0.455, P=.006) in women but not in men. Serum resistin level only correlated negatively with high-density lipoprotein cholesterol (HDL-C) level in men (gamma=-0.347, P=.038); there was no correlation between serum resistin level and lipid profiles in women. Multiple linear regression analysis using the logarithm of resistin as a dependent variable revealed that only HDL-C level (beta=-.058, P=.019) was an independent significant predictor for resistin in men; however, the analysis revealed that HDL-C level (beta=-.044, P=.029) and HOMA (beta=-.719, P=.004) were independent significant predictors for resistin in women. In conclusion, resistin is not related to adiposity, blood pressure, insulin resistance, fasting plasma glucose level, and most lipid profiles. Resistin correlates negatively with HDL-C level for both sexes. The role of resistin in metabolic syndrome warrants further investigation.