A paradox:Insulin inhibits expression and secretion of resistin which induces insulin resistance

AIM: To confirm whether insulin regulates resistinexpression and secretion during differentiation of 3T3-L1preadipocytes and the relationship of resistin with insulinresistance both in vivo and in vitro.METHODS: Supernatant resistin was measured duringdifferentiation of 3T3-L1 preadipocytes. L6 rat myoblastsand hepatoma cell line H4IIE were used to confirm thecellular function of resistin. Diet-induced obese ratswere used as an insulin resistance model to study therelationship of resistin with insulin resistance.RESULTS: Resistin expression and secretion wereenhanced during differentiation 3T3-L1 preadipocytes.This cellular differentiation stimulated resistin expressionand secretion, but was suppressed by insulin. Resistinalso induced insulin resistance in H4IIE hepatocytes andL6 myoblasts. In diet-induced obese rats, serum resistinlevels were negatively correlated with insulin sensitivity,but not with serum insulin.CONCLUSION: Insulin can inhibit resistin expressionand secretion in vitro, but insulin is not a major regulatorof resistin in vivo . Fat tissue mass affects insulinsensitivity by altering the expression and secretion ofresistin.

Resistin does not down-regulate the transcription of insulin receptor promoter

Objective: To detect the effect of resistin on the transcription of insulin receptor promoter. Methods: Luciferase reporter gene was fused downstream of human insulin receptor promoter and the enzymatic activity of luciferase was determined in the presence or absence of resistin. The resistin expressed with plasmid was stained with antibody against Myc tag which was in frame fused with resistin coding sequence, and then imaged with confocal microscopy. Results: The treatment of pIRP-LUC transfected cells with recombinant resistin did not result in significant difference in the enzymatic activity of luciferase compared to the untreated cells. Cell staining showed that green fluorescence could be observed in the cytoplasm, but not in the nucleus. Conclusion: The results suggest that the endogenous resistin may functionally locate in the cytoplasm, but does not enter the nucleus and not down-regulate the transcription of insulin receptor promoter.

Over expression of resistin in adipose tissue of the obese induces insulin resistance

AIM: To compare resistin mRNA expression in subcutaneous adipose tissue (SAT) and its correlation with insulin resistance (IR) in postmenopausal obese women. METHODS: A total of 68 postmenopausal women (non obese = 34 and obese = 34) were enrolled for the study. The women of the two groups were age matched (49-70 years). Fasting blood samples were collected at admission and abdominal SAT was obtained during surgery for gall bladder stones or hysterectomy. Physical parameters [age, height, weight, body mass index (BMI)] were measured. Biochemical (plasma insulin and plasma glucose) parameters were estimated by enzymatic methods. RNA was isolated by the Trizol method.SAT resistin mRNA expression was done by real time- reverse transcription polymerase chain reaction (RT-PCR) by using Quanti Tect SYBR Green RT-PCR master mix. Data was analyzed using independent Student's t test, correlation and simple linear regression analysis. RESULTS: The mean weight (52.81 ± 8.04 kg vs 79.56 ± 9.91 kg; P < 0.001), BMI (20.23 ± 3.05 kg/m 2 vs 32.19 ± 4.86 kg/m 2 ; P < 0.001), insulin (8.47 ± 3.24 U/mL vs 14.67 ± 2.18 U/mL; P < 0.001), glucose (97.44 ± 11.31 mg/dL vs 109.67 ± 8.02 mg/dL; P < 0.001) and homeostasis model assessment index (2.01 ± 0.73 vs 3.96 ± 0.61; P < 0.001) were significantly higher in postmenopausal obese women compared to postmenopausal non obese women. The mean serum resistin level was also significantly higher in postmeno-pausal obese women compared to postmenopausal non obese women (9.05 ± 5.15 vs 13.92 ± 6.32, P < 0.001). Furthermore, the mean SAT resistin mRNA expression was also significantly (0.023 ± 0.008 vs 0.036 ± 0.009; P < 0.001) higher and over expressed 1.62 fold (upregulated) in postmenopausal obese women compared to postmenopausal non obese women. In postmeno-pausal obese women, the relative SAT resistin mRNA expression showed positive (direct) and significant correlation with BMI (r = 0.78, P < 0.001) and serum resistin (r = 0.76, P < 0.001). Furthermore, the SAT resistin mRNA expression in postmenopausal obese women also showed significant and direct association (r = 0.45, P < 0.01) with IR, while in postmenopausal non obese women it did not show any association (r = -0.04, P > 0.05). CONCLUSION: Increased SAT resistin mRNA expres-sion probably leads to inducing insulin resistance and thus may be associated with obesity-related disorders in postmenopausal obese women.

The Expression of Resistin in Adipose Tissues of Patients with Polycystic Ovary Syndrome and Insulin Resistance

The relationship between the expression of resistin in polycystic ovary syndrome （PCOS） and insulin resistance was investigated. The plasma resistin concentrations in 35 patients with PCOS and 40 controls were measured by ELISA. Luteinizing hormone （LH）, follicle-stimulating hormone （FSH）, and fasting insulin （FIN） were tested by radioimmunoassay. Insulin resistance index （HOMA-IR） was calculated. Fasting plasma glucose （FPG） was determined by oxidase test. Western blot and reverse transcriptase PCR （RT-PCR） methods were used to detect the expression of resistin in adipose tissues. The levels of plasma resistin, LH, LH/FSH and FIN and HOMA-IR in patients with PCOS were significantly higher than those in control group （all P〈0.05）. Plasma resistin was correlated positively with FPG, FIN, HOMA-IR, LH and LH/FSH （r=0.56, 0.60, 0.65, 0.48, and 0.42 respectively）. Resistin protein and mRNA expression levels in patients with PCOS were significantly higher than those in normal tissues （all P〈0.01）. It was concluded that resistin might be involved in the pathogenesis of insulin resistance of PCOS.

人resistin基因原核表达载体构建和表达

【目的】构建人resistin基因原核表达载体并观察其表达,为开展对resistin的研究打下实验基础。【方法】酚氯仿一步法从一位2型糖尿病合并胆管癌患者腹壁皮下脂肪组织抽取总RNA,RT-PCR法扩增出re-sistin基因cDNA,经测序后,PCR产物亚克隆入T载体,用EcoRI和KpnI分别酶切重组T质粒和原核表达载体pGENKS,然后resistin基因片段和表达载体通过T4DNA连接酶进行定向连接,用核酸内切酶EcoRI、KpnI酶切和测序方法鉴定出重组表达质粒。重组表达质粒转化大肠杆菌JM109,经1mmol/LIPTG在32℃诱导表达2h,裂解细菌,进行PAGE凝胶电泳鉴定融合蛋白的表达。【结果】RT-PCR扩增产物分子大小为327bp,序列分析表明为人resistin基因完整编码区。PCR产物与T载体连接、转化大肠杆菌后,从细菌质粒中酶切回收了目的片段。重组表达质粒经EcoRI和KpnI双酶切后能产生出327bp、4980bp大小的两个片段,序列分析表明重组表达质粒包含人resistin基因完整编码区,基因编码无移位,PAGE凝胶电泳表明在细菌裂解上清有分子质量为39.5kD的融合蛋白。【结论】成功构建了人resistin基因原核表达载体,且构建的载体能表达出含目的蛋白的融合蛋白,为下一步研究打下了实验基础。

枸杞多糖对2型糖尿病胰岛素抵抗模型大鼠resistin基因表达的影响

观察枸杞多糖(LBP)对高脂膳食加链脲佐菌素(STZ)诱导的2型糖尿病(2-DM)大鼠胰岛素抵抗指数及肾周脂肪组织抵抗素(resistin)基因表达的影响。选用高脂饲料加STZ建立2-DM胰岛素抵抗大鼠模型,将造模大鼠随机分为模型对照组、罗格列酮组和LBP高、中、低剂量组(80mg/kg、40mg/kg、20mg/kg),每组各10只,另选10只大鼠为正常对照组。各组灌胃8周后,空腹取材,RT-PCR法检测肾周脂肪组织resistin基因mRNA水平,放射免疫法测定空腹胰岛素并计算胰岛素抵抗指数(insulin resistance index,IRI)。结果表明,与模型组比较,罗格列酮组及LBP各剂量组均能显著降低2-DM大鼠肾周脂肪组织resistin基因mRNA表达,降低IRI。说明LBP具有改善2-DM大鼠胰岛素抵抗的作用。

西洋参活性部位对胰岛素抵抗大鼠resistin基因mRNA表达的影响

目的:观察西洋参治疗胰岛素抵抗(Insulin Resistance,IR)大鼠活性部位对Resistin基因表达的影响。方法:通过早期药效学试验证明,西洋参根部60%洗脱部分和30%洗脱部分为有效部位。本实验采用高脂饲料喂养加链脲佐菌素法复制IR大鼠(SD)的动物模型,造模成功后,将大鼠随机分为模型组、罗格列酮组、西洋参60%洗脱组、西洋参30%洗脱组。给药4周后,以RT-PCR法检测附睾周围白色脂肪组织中Resistin-mRNA的表达。结果:与模型组比较,各给药组大鼠脂肪组织中Resistin基因mRNA的表达均降低,其中以西洋参60%洗脱组作用最强,与模型组比较有极显著差异(P<0.01),西洋参30%洗脱组和罗格列酮组与模型组比较差异显著(P<0.05)。结论:西洋参可降低IR大鼠脂肪组织中Resistin基因的表达;西洋参60%洗脱部位降低Resistin基因表达的作用最明显。

地黄水提液对2型糖尿病大鼠胰岛素抵抗及resistin基因mRNA和蛋白表达的影响

目的:探讨中药地黄水提液对2型糖尿病大鼠糖脂代谢和resistin基因表达的影响。方法:Wistar大鼠喂以高热量饲料加链脲佐菌素建立2型糖尿病大鼠模型,随机分为正常对照组、2型糖尿病模型组、地黄高、中、低剂量治疗组。8周后,以RT-PCR法检测大网膜脂肪组织resistin基因mRNA的表达,以SDS-PAGE检测其蛋白的表达。同时观察空腹血糖、空腹血胰岛素、血脂的含量和胰岛素抵抗指数的变化,研究不同剂量地黄水提液对上述各指标的影响。结果:地黄治疗组大鼠较模型组大鼠resistin基因mRNA和蛋白表达显著降低(P<0.05)。各治疗组FPG,FINS,TG,LDL,CH的含量及IR显著降低(P<0.05),而HDL则显著升高(P<0.05)。结论:地黄水提液通过抑制脂肪组织抵抗素基因的表达,降低血胰岛素抵抗水平、改善脂代谢紊乱,从而降低2型糖尿病大鼠血糖。

resistin在妊娠期糖尿病患者胎盘组织的表达及意义

目的:探讨妊娠期糖尿病(GDM)患者胎盘组织抵抗素(resistin)的表达及在妊娠期糖尿病发病过程中的意义。方法:用逆转录聚合酶链反应(RT-PCR)及免疫印迹法(Western blot)检测18例妊娠期糖尿病患者(妊娠期糖尿病组)和18例正常晚期妊娠妇女(正常对照组)胎盘组织resistin mRNA和resistin蛋白的表达,同时检测体重指数(BMI)、空腹血糖水平(FPG)、空腹胰岛素水平(FINS)、血脂水平和胰岛素抵抗指数(HO- MA-IR)。结果:(1)GDM组甘油三酯(TG)、FPG、FINS及HOMA-IR的水平明显高于对照组(P<0.05或P<0.01);(2)两组胎盘组织中均可检测到resistin mRNA和resistin蛋白表达。GDM组的resistin mRNA表达水平及蛋白表达水平均高于对照组(P<0.01,P<0.05);(3)GDM组HOMA-IR水平与胎盘组织resistin mRNA表达水平(r=0.621,P<0.05)、resistin蛋白表达水平(r=0.739,P<0.01)及TG(r=0.786,P<0.01)呈正相关;GDM组TG水平与胎盘组织resistin mRNA表达水平(r=0.592,P<0.05)、resistin蛋白表达水平(r=0.546,P<0.05)呈正相关。正常妊娠组则无相关性。结论:胎盘组织分泌的resistin与GDM胰岛素抵抗密切相关,胎盘resistin表达异常可能参与了GDM的发病过程。

血清Resistin水平与2型糖尿病大血管并发症的关系

目的:探讨血清Resistin水平与2型糖尿病(T2DM)大血管并发症(DA)的关系。方法:采用酶联免疫法测定T2DM患者128例眼其中85例并发高血压、冠心病、脑梗塞者为DA穴+雪组演和对照组61例的空腹血清Resistin水平。结果:DA穴+雪组血清Resistin水平升高穴P<0.05雪。采用相关分析发现,血清Resistin浓度与BMI、Waist、WHR、BF%、TG、ApoB、FINS、SBP、DBP呈显著正相关穴P均<0.05雪,与ISI呈显著负相关穴P<0.01雪,男性Resistin水平与T呈正相关穴P<0.001雪。采用多元逐步回归分析发现,BF%、SEX、FINS、Waist为影响Resistin最为显著的因素(R2=0.78)。结论:血清高Resistin水平与高胰岛素血症的相关性提示,Resistin可能在2型DM及其DA的发病中起一定作用。

Resistin结合多肽对胰岛β细胞株RINm5F分泌功能的影响(英文)

目的先前研究已显示resistin结合多肽(RBP)能拮抗resistin对脂肪细胞脂质代谢和内分泌功能的调节作用。本研究试图阐明RBP对胰岛β细胞株RINm5F分泌功能的影响。方法以不同水平RBP(10-10,10-11,10-12mol/L)与RINm5F共培养30min、60min、2h后取上清,ELISA法测其胰岛素,RT-PCR法检测细胞中葡萄糖转运子2(GLUT2)mRNA表达水平,Western blotting法检测细胞中GLUT2的蛋白水平,并采用FURA-3/AM钙荧光染色法检测胰岛素分泌的重要启动因素:细胞内钙水平。结果RBP在10-12mol/L时干预2h,不影响胰岛β细胞株RINm5F的细胞活性,但能显著刺激胰岛素分泌。RBP为10-12mol/L时干预2h,细胞内钙明显增多。在Resistin刺激下,GLUT2mRNA水平和蛋白水平均显著上调。结论RBP能促进RINm5F细胞株胰岛素的分泌,其可能机制是RBP上调了GLUT2的表达,进而增加了细胞内钙的水平,最终导致胰岛素分泌增加。

抵挡芪桂汤对胰岛素抵抗大鼠血清Resistin、ROS含量的影响

目的通过观察抵当芪桂汤对胰岛素抵抗(IR)大鼠血清Resistin、ROS的含量影响,探讨该方防治糖尿病的作用机理。方法将70只SD大鼠随机选取10只作为空白组,其余60只大鼠给予高糖、高脂饲料喂养,于第8周末禁食不禁水,次日早一次性腹腔注射链脲佐菌素(STZ)35 mg/kg造模,72 h后测其随机血糖、尿糖,血糖≥16.9 mmol/L、尿糖(3+)或以上为造模成功。将成模大鼠随机分为模型组、中药组、西药组和中西药组,给予相应干预。在干预第8周末检测大鼠血清中Resistin、ROS的含量。结果干预8周后,与模型组比较,各给药组大鼠血清Resistin、ROS含量均有不同程度降低,其中以中药组、中西药组最为明显(P<0.05)。结论常规剂量抵当芪桂汤及中西药结合治疗能够降低高脂高糖饮食合并STZ诱导胰岛素抵抗大鼠血清Resistin、ROS含量。

抵抗素调控机制及其与慢性疾病关系的研究现状

抵抗素是在小鼠脂肪细胞中发现的激素,在炎症、代谢、免疫性疾病、慢性疾病中发挥重要作用。该文就抵抗素调控机制及其与慢性肾脏病、心血管疾病、肥胖及糖尿病、癌症的关系作一综述。

PLASMA RESISTIN LEVELS AND SINGLE-NUCLEOTIDE POLYMORPHISMS IN RESISTIN GENE 5 FLANKING REGION IN PATIENTS WITH STROKE

Objective To analyze the role of resistin in insulin resistance (IR) through investigating the variation of plasma resistin levels and single-nucleotide polymorphisms (SNPs) in resistin gene 5’ flanking region in stroke patients.Methods In 103 atherothrombotic cerebral infarction (ACI) patients, 85 lacunar infarction (LI) patients, 70 intracerebral hemorrhage (ICH) patients, and 86 healthy controls, plasma resistin and insulin levels were measured by ELISA , SNPs in resistin gene 5’ flanking region were detected by PCR and direct DNA sequencing. The subjects’ body height and weight, the body mass index, quantitative insulin sensitivity check index (QUICKI), blood pressure, and the concentration of fasting plasma glucose, triglyceride, total cholesterol, creatinine, low-density lipoprotein, and high-density lipoprotein were also determined. Results QUICKI was significantly lower in the ACI and ICH patients (0.316±0.037 and 0.309±0.032, respectively) than that in the controls (0.342±0.043, P<0.001), while plasma resistin level was significantly higher in the ACI and ICH patients (6.36±3.79 and 7.15±4.27 ng/mL, respectively) than that in the controls (5.28±2.56 ng/mL, P<0.05), but such difference was not observed in the LI patients compared with controls. There was a statistically negative correlation between plasma resistin level with QUICKI (r=-0.228, P<0.001). The distributions of allele and genotype frequencies of resistin gene -420C>G and -537A>C SNPs were not significantly different among the different groups, and those SNPs were not correlated with other clinical and biochemical parameters.Conclusions Plasma resistin is associated with stroke by participating in the development of IR. The SNPs in resistin gene 5’ flanking region has no impact on the plasma resistin level.

Resistin levels of serum and follicular fluid in non-obese patients with polycystic ovary syndrome during IVF cycles

Objectives: To measure serum and follicular resistin, steroids hormone levels in women with PCOS (polycystic ovary syndrome) (BMI (body mass index)<25 kg/m2), to assess possible correlations of resistin to hormonal and metabolic parameters and to analyze the clinical outcomes of in vitro fertilization-embryo transfer (IVF-ET) in women with PCOS and tubal infertility. Study design: We analyzed the clinical outcomes of IVF-ET in women with PCOS (BMI<25 kg/m2) and tubal infertility during the years 2002 to 2004 and compared the serum and follicular fluid resistin levels, estradiol (E2), progesterone (P), testosterone (T) levels in 20 PCOS and 20 healthy, age-matched women without PCOS during IVF-stimulated cycles. The correlations between the resistin levels and the outcomes of IVF-ET were evaluated. Results: No significant differences in resistin levels of either serum or follicular fluid between PCOS and control group were found. However, resistin levels in serum were higher than that in follicular fluid in both groups. Multiple regression analysis showed that resistin levels in serum did not correlate with BMI, estradiol, LH (luteinizing hormone) and insulin level in fasting blood. No significant correlations were found between follicular fluid reisistin levels and fertilization rate, implantation rate, clinical pregnancy rate or early miscarriage rate in both PCOS and control groups. Conclusion: Our results show that resistin does not have correlation with the hormonal and metabolic parameters as well as the outcomes of IVF. These data suggest that resistin is unlikely to be a local determinant factor in steroidogenesis and growth and maturation of oocytes during IVF-ET in lean women with PCOS.

Expression of Resistin Protein in Normal Human Subcutaneous Adipose Tissue and Pregnant Women Subcutaneous Adipose Tissue and Placenta

The expression of resistin protein in normal human abdominal, thigh, pregnant women abdominal, non-pregnant women abdominal subcutaneous adipose tissue and placenta and the relationship between obesity, type 2 diabetes mellitus （T2DM）, pregnant physiological insulin resistance （IR） and gestational diabetes mellitus （GDM） was investigated. The expression of resistin protein in normal human abdominal, thigh, pregnant women abdominal, non-pregnant women abdominal subcutaneous adipose tissue and placenta was detected by using Western blotting method. Fasting serum glucose concentration was measured by glucose oxidase assay. Serum cholesterol （CHOL）, serum triglycerides （TG）, serum HDL cholesterol （HDL-C） and serum LDL cholesterol （LDL-C） were determined by full automatic biochemical instrument. Fasting insulin was measured by enzyme immunoassay to calculate insulin resistance index （IRI）. Height, weight, systolic blood pressure （SBP） and diastolic blood pressure （DBP） were measured to calculate body mass index （BMI） and body fat percentage （BF%）. Resistin protein expression in pregnant women placental tissue （67 905±8441） （arbitrary A values） was much higher than that in subcutaneous adipose tissue in pregnant women abdomen （40 718 ± 3818, P〈 0. 01 ）, non-pregnant women abdomen （38 288±2084, P〈0.01）, normal human abdomen （39 421±6087, P〈0.01） and thigh （14 942 ±6706, P〈0.001） respectively. The resistin expression in abdominal subcutaneous adipose tissue showed no significant difference among pregnant, non-pregnant women and normal human, but much higher than that in thigh subcutaneous adipose tissue （P〈0. 001）. Pearson analysis revealed that resistin protein was correlated with BMI （r=0.42）, fasting insulin concentration （r=0.38）, IRI （r=0.34）, BF% （r=0.43） andfasting glucose （r=0.39）, but not with blood pressure, CHOL, TG, HDL-C and LDL-C. It was suggested that resistin protein expression in human abdominal subcutaneous adipose tissue was much higher than that in human thigh subcutaneous adipose tissue. Resistin was closely related with central obesity, leading to IR, subsequently obesity and T2DM. Resistin protein expression in placental tissue was much higher than that in subcutaneous adipose tissue in normal human abdomen, pregnant abdomen, non-pregnant women abdomen and thigh. It was indicated that resistin protein could be secreted from human placental tissue. Resistin might be one of the factors that lead to pregnant physiological IR and GDM.

多囊卵巢综合征患者妊娠早期血清Resistin水平与不良妊娠结局

目的:探讨多囊卵巢综合征(PCOS)孕妇妊娠早期血清抵抗素(Resistin)表达特征及与不良妊娠关系。方法:选取54例PCOS孕妇和100例健康孕妇分别作为病例组与对照组。在孕早期行血清Resistin、性激素结合球蛋白(SHBG)、空腹血糖(FPG)、空腹胰岛素(FINS)水平检测并分析与不良妊娠结局关系。结果:病例组血清Resistin、HOMA-IR值均高于对照组,SHBG水平低于对照组(P<0.05)。病例组妊娠结局良好者的Resistin、HOMA-IR水平均低于不良者,SHBG水平高于不良者(P<0.05)。病例组不良妊娠结局与妊娠早期血清Resistin、HOMA-IR水平呈正相关(r=0.416、0.316,P<0.05),与血清SHBG水平呈负相关(r=-0.307,P<0.05),血清Resistin水平相关程度最强。结论:PCOS孕妇妊娠早期血清Resistin水平升高且与妊娠并发症、不良妊娠结局有正相关关系,SHBG和HOMA-IR也可作为预测PCOS患者不良妊娠结局的参考指标。

Obesity, insulin resistance, adipocytokines and breast cancer: New biomarkers and attractive therapeutic targets

Worldwide, breast cancer(BC) represents the most common type of non-skin human malignancy and the second leading cause of cancer-related deaths amid women in Western countries. Obesity and its metabolic complications have rapidly become major global health issues and are associated with increased risk for cancer, especially BC in postmenopausal women. Adipose tissue is considered as a genuine endocrine organ secreting a variety of bioactive adipokines, such as leptin, adiponectin, resistin and nicotinamide phosphoribosyltransferase/visfatin. Recent evidence has indicated that the constellation of obesity, insulin resistance and adipokines is associated with the risk and prognosis of postmenopausal BC. Direct evidence is growing rapidly supporting the stimulating and/or inhibiting role of adipokines in the process of development and progression of BC. Adipokines could exert their effects on the normal and neoplastic mammary tissue by endocrine, paracrine and autocrine mechanisms. Recent studies support a role of adipokines as novel risk factors and potential diagnostic and prognostic biomarkers in BC. This editorial aims at providing important insights into the potential pathophysiological mechanisms linking adipokines to the etiopathogenesis of BC in the context of a dysfunctionaladipose tissue and insulin resistance in obesity. A better understanding of these mechanisms may be important for the development of attractive preventive and therapeutic strategies against obesity-related breast malignancy.

Adipose tissue resistin gene expression in DIO and DR rats

Objective： To investigate the expression of resistin gene in diet-induced obesity （DIO） and diet resistance （DR） rats. Methods： DIO and DR models were prepared with male SD rats after 6 weeks feeding by a diet of relatively high fat, sucrose, and caloric content （HE diet）. Body-weight, fat mass, and the concentration of serum insulin were measured, and the expression of resistin and Peroxisome proliferator-activated receptory-7（PPAR-7） gene in whit adipose tissue （WAT） was also detected by RT-PCR. Results： ① Body weight, fat mass and the concentration of serum insulin were significantly increased in DIO rats and decreased in DR rats. ② The expression of resistin and PPAR7 gene was upregulated in DIO group and supressed in DR group, but the expression of resistin was not detectable in all samples within three groups. Conclusion： Resistin may serve as a link between obesity and insulin resistance, but the individual difference is enormous.

黄连解毒汤对胰岛素抵抗大鼠瘦素和抵抗素的影响

目的探讨黄连解毒汤对胰岛素抵抗大鼠脂质代谢、瘦素和抵抗素的影响。方法观察黄连解毒汤对实验性胰岛素抵抗大鼠的血脂[甘油三酯(TG)、总胆固醇(TC)、高密度脂蛋白胆固醇(HDL-C)、载脂蛋白A1(apoA1)、载脂蛋白B(apoB)、游离脂肪酸(FFA)]、骨骼肌组织甘油三酯(mTG)、糖耐量(OGTT)、空腹血糖(FBG)、血清胰岛素(INS)及体重的变化,用ELISA方法检测血清瘦素和抵抗素的含量。结果与模型组比较,黄连解毒汤组大鼠血清TC、TG、apoB、FFA、mTG及FBG水平均明显降低,而HDL-C与apoA1水平显著升高,OGTT改善,大鼠体重减轻,瘦素和抵抗素明显降低(P<0.05或P<0.01)。结论黄连解毒汤能调节胰岛素抵抗大鼠脂质代谢,同时能降低瘦素和抵抗素的水平,这可能与其改善胰岛素抵抗有关。