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.

Salivary resistin level and its association with insulin resistance in obese individuals

The escalating global burden of type 2 diabetes mellitus necessitates the implementation of strategies that are both more reliable and faster in order to improve the early identification of insulin resistance(IR)in high-risk groups,including overweight and obese individuals.The use of salivary biomarkers offers a promising alternative to serum collection because it is safer,more comfortable,and less painful to obtain saliva samples.As obesity is the foremost contributory factor in IR development,the adipocytokines such as leptin,adiponectin,resistin,and visfatin secreted from the adipose tissue have been studied as potential reliable biomarkers for IR.Measurement of salivary adipokines as predictors for IR has attracted widespread attention because of the strong correlation between their blood and salivary concentrations.One of the adipokines that is closely related to IR is resistin.However,there are conflicting findings on resistin’s potential role as an etiological link between obesity and IR and the reliability of measuring salivary resistin as a biomarker for IR.Hence this study reviewed the available evidence on the potential use of salivary resistin as a biomarker for IR in order to attempt to gain a better understanding of the role of resistin in the development of IR in obese individuals.

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.

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.

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。

Serum resistin and the risk for hepatocellular carcinoma in diabetic patients

Hepatocellular carcinoma(HCC),the predominant type of liver cancer,is a major contributor to cancer-related fatalities across the globe.Diabetes has been identified as a significant risk factor for HCC,with recent research indicating that the hormone resistin could be involved in the onset and advancement of HCC in diabetic individuals.Resistin is a hormone that is known to be involved in inflammation and insulin resistance.Patients with HCC have been observed to exhibit increased resistin levels,which could be correlated with more severe disease stages and unfavourable prognoses.Nevertheless,the exact processes through which resistin influences the development and progression of HCC in diabetic patients remain unclear.This article aims to examine the existing literature on the possible use of resistin levels as a biomarker for HCC development and monitoring.Furthermore,it reviews the possible pathways of HCC initiation due to elevated resistin and offers new perspectives on comprehending the fundamen-tal mechanisms of HCC in diabetic patients.Gaining a better understanding of these processes may yield valuable insights into HCC’s development and progression,as well as identify possible avenues for prevention and therapy.

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。

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.

低升糖指数饮食+运动干预对肥胖人群脂联素和胰岛素抵抗指数的影响

目的探讨低升糖指数饮食+运动干预对肥胖人群脂联素和胰岛素抵抗指数的影响。方法选取东莞市南城医院2022年1月—2023年6月身体质量指数(body mass index,BMI)≥28 kg/m^(2)肥胖人群100例作为观察组,并选取同时间段BMI 18.5~24 kg/m^(2)的正常体质量人群100例作为对照组。2组均行健康检查,并比较2组的腰臀比、体脂分布百分比、脂联素、总胆固醇、三酰甘油、胰岛素、胰岛素抵抗指数的差异,同时采取Pearson法分析脂联素与各指标的相关性。对观察组展开低升糖指数饮食+运动干预,比较干预前与干预4个月后各指标的变化。结果观察组腰臀比[(1.53±0.32)vs.(0.88±0.12)]、体脂分布百分比[(36.83±7.63)%vs.(27.12±4.21)%]高于对照组,脂联素[(0.68±0.16)mg/L vs.(1.21±0.22)mg/L]低于对照组,差异有统计学意义(P<0.05)。观察组总胆固醇、三酰甘油、胰岛素、胰岛素抵抗指数均高于对照组(P<0.05)。通过Pearson法分析发现,脂联素与腰臀比、体脂分布百分比、总胆固醇、三酰甘油、胰岛素、胰岛素抵抗指数存在负相关性(P<0.05)。观察组干预后腰臀比、体脂分布百分比、总胆固醇、三酰甘油、胰岛素、胰岛素抵抗指数均低于干预前,脂联素高于干预前,差异有统计学意义(P<0.05)。结论肥胖人群与正常体质量人群相比,存在脂联素下降、胰岛素抵抗升高的特点,且脂联素与腰臀比、体脂分布百分比、总胆固醇、三酰甘油、胰岛素、胰岛素抵抗指数存在负相关性。通过低升糖指数饮食与运动干预可以改善肥胖人群的血脂水平与胰岛素抵抗状况。

营养干预对肥胖型多囊卵巢综合征患者内分泌及妊娠成功率的影响

目的探讨药物治疗基础上联合营养干预对肥胖型多囊卵巢综合征(PCOS)血糖、生殖激素及妊娠成功率的影响。方法选取2021年1月至2023年12月收治的有生育需求肥胖型PCOS患者118例。按照随机数字表法分为对照组与观察组,每组59例。观察组给予药物联合营养干预治疗,对照组给予单纯药物治疗。2组均连续治疗3个月经周期。观察并对比2组治疗前后体质量指数(BMI)、腰臀比、血糖水平、胰岛素抵抗指数、生殖激素水平及排卵和妊娠成功率。结果治疗后,2组空腹血糖、餐后2 h血糖、胰岛素水平、胰岛素抵抗指数、黄体生成素、睾酮水平均较治疗前降低,且观察组低于对照组(P<0.05)。治疗后,2组BMI、腰臀比均较治疗前明显降低,观察组BMI较对照组明显降低(P<0.05,P<0.01),但腰臀比组间比较差异无统计学意义(P>0.05)。治疗后,2组促卵泡生成素高于治疗前,且观察组高于对照组(P<0.05,P<0.01)。2组排卵成功率比较差异无统计学意义(P>0.05);观察组妊娠成功率[49.15%(29/59)]高于对照组[32.20(19/59)],差异有统计学意义(P<0.05)。结论药物治疗基础上联合营养干预能够明显降低肥胖型PCOS患者的BMI,改善机体胰岛素抵抗的状态,缓解肥胖状态,能够正向改善生殖激素水平,从而提高肥胖型PCOS患者成功受孕率。

血清抵抗素水平与肥胖及2型糖尿病的关系

目的 研究血清抵抗素水平与肥胖、2型糖尿病 (T2DM )和胰岛素抵抗 (IR)的关系。 方法 用酶免疫测定法检测 31例单纯肥胖、2 7例T2DM及 30名正常人空腹血清抵抗素水平。 结果 单纯肥胖组、T2DM组及正常对照组空腹抵抗素分别为 ( 4 1± 13)、( 4 3± 11)和 ( 5 3± 7) μg/L。单纯肥胖组和T2DM组血清抵抗素浓度均低于正常对照组 (P <0 0 1)。空腹血清抵抗素与体质指数(BMI)、胰岛素抵抗指数 (HOMA IR)分别呈负相关 (r =- 0 2 92及 - 0 319,P <0 0 1) ,与空腹胰岛素、腰围和体脂百分比 (BF % )也呈负相关 (r =- 0 2 5 9,- 0 2 31及 - 0 2 39,P <0 0 5 )。多元逐步回归分析显示 ,HOMA IR为影响抵抗素最为显著的因素 (R2 =0 0 86 )。 结论 肥胖及T2DM患者血清抵抗素水平偏低。血清抵抗素与BMI、体脂百分比、腰围、空腹胰岛素和HOMA IR呈负相关。

肥胖人群脂联素、抵抗素和胰岛素抵抗水平的研究

目的探讨肥胖患者血清脂联素、抵抗素和胰岛素抵抗水平的变化及意义。方法分别测定106例肥胖者和107名健康对照者的体重指数(BMI)、腰围、臀围、空腹胰岛素、空腹血糖、血脂、脂联素和抵抗素水平,计算胰岛素抵抗指数(HOMA-IRI)。结果肥胖者的体重指数(BMI)、体脂分布百分比(BF)、HOMA-IRI、抵抗素、脂联素、总胆固醇(TC)、载脂蛋白B(apo B)与健康对照组比较,差异均有统计学意义(P<0.01、P<0.05)。脂联素和抵抗素均与BMI、BF和HOMA-IRI呈正相关([脂联素:相关系数(r)分别为0.439、0.236、0.398,P均<0.01;抵抗素:r分别为0.296(P<0.01)、0.175(P<0.05)、0.827(P<0.01)],抵抗素与腰臀比(WHR)呈正相关(r=0.169,P<0.05)。结论脂联素能较好地预测BMI和HOMA-IRI,抵抗素能较好地预测BMI。脂联素与抵抗素水平的变化可能导致肥胖和胰岛素抵抗,在向糖尿病的发生发展过程中起了一定作用。

抵抗素与胰岛素抵抗、肥胖及2型糖尿病的关系

近十年来,抵抗素作为新近发现的一种脂肪细胞因子,被认为是联系肥胖、胰岛素抵抗及2型糖尿病的一种激素。多数动物实验发现抵抗素可引起胰岛素抵抗,且与肥胖、糖尿病有关,但目前临床研究结果尚存争议,并且对于抵抗素在人体内确切的生理作用机制尚不明了。本文就抵抗素与胰岛素抵抗、肥胖及2型糖尿病的关系研究进展进行综述。

代谢综合征患者血清抵抗素与血脂、肥胖和胰岛素抵抗关系的研究

目的:探讨代谢综合征患者血清抵抗素水平与血脂、肥胖和胰岛素抵抗的关系。方法: 60 例代谢综合征患者和28 例年龄相匹配的正常对照者,按体重指数将代谢综合征患者分为肥胖组和非肥胖组。采用ELISA方法测定受试者空腹血清抵抗素和瘦素水平,同时检测其身高、体重、腰围、臀围、血压、血糖、血脂及胰岛素水平,并计算体重指数(BMI)、腰臀比(WHR)和胰岛素抵抗指数(HOMA)。结果:代谢综合征患者肥胖组和正常对照组相比其血清抵抗素水平明显升高(28.28±11.7μg/L与19.44±5.79μg/L,P<0.01);非肥胖组和正常对照组相比其血清抵抗素水平明显升高(26.14±11.9μg/L与19.44±5.79μg/L,P<0.05)。肥胖组和正常对照组相比其血清瘦素水平明显升高(1.47±0.57μg/L与0.31±0.13μg/L,P<0.01);非肥胖组和正常对照组相比其血清瘦素水平明显升高(1.35±0.57μg/L与0.31±0.13μg/L,P<0.01)。肥胖组和非肥胖组相比其血清抵抗素、瘦素水平无显著差异。相关分析显示空腹抵抗素水平与腰臀比、空腹胰岛素、胰岛素抵抗指数呈显著正相关(分别为r=0.22,0.22,0.19;P<0.05);与体重指数、腰围、臀围、瘦素呈显著正相关(分别为r=0.31,0.32,0.36,0.28;P<0.01);而与收缩压、舒张压、总胆固醇、甘油三酯、低密度脂蛋白胆固醇(LDL C)、血?

单纯性肥胖患者血清瘦素、抵抗素和脂联素水平的研究

目的:探讨单纯性肥胖患者血清瘦素、抵抗素和脂联素水平的变化及意义。方法:分别测定单纯性肥胖组患者和正常对照者的体质指数(BM I)、腰围(WC)、臀围、空腹胰岛素(FINS)、空腹血糖(FBG)、血脂、瘦素、抵抗素和脂联素的水平,计算胰岛素抵抗指数(HOMA-IR)。结果:①与正常对照组相比,单纯性肥胖组脂联素水平明显降低,瘦素及抵抗素水平明显升高(P<0.01)。②瘦素和抵抗素均与BM I、WC、FINS和HOMA-IR呈正相关,与脂联素呈负相关;脂联素则仅与高密度脂蛋白呈正相关,与BM I、WC、FBG、FINS、HOMA-IR、三酰甘油、低密度脂蛋白呈负相关;瘦素与抵抗素呈正相关,而脂联素与瘦素及抵抗素呈负相关。③脂联素和抵抗素能较好地预测BM I和WC。结论:脂联素降低、瘦素和抵抗素升高易导致中心性肥胖和胰岛素抵抗。脂联素、抵抗素水平可能是肥胖发生的预测指标。

2型糖尿病患者血浆抵抗素水平与脂联素和胰岛素抵抗的关系

目的 :探讨 2型糖尿病和 2型糖尿病伴肥胖症患者血浆抵抗素与脂联素和胰岛素抵抗之间的关系。方法 :对 88例居住在武汉检查者 (正常对照 2 8例 ,2型糖尿病 30例 ,2型糖尿病合并肥胖症 30例 )同时采集病史、进行体格检查并留取血浆 ,测定其血糖、胰岛素、血脂、瘦素、脂联素和抵抗素的水平。结果 :简单相关分析提示抵抗素与体重指数、腰臀比、空腹及餐后 1h和 2h的血糖、甘油三酯和胰岛素抵抗正相关 ,与脂联素负相关 ;校正其它参数 ,抵抗素的水平与体重指数呈正相关 ,与脂联素呈负相关。结论 :抵抗素和脂联素与肥胖症和 2型糖尿病的发生有关。

老年2型糖尿病患者血清抵抗素水平与胰岛素抵抗的相关性研究

目的探讨抵抗素在老年2型糖尿病患者中的作用及其与肥胖、胰岛素抵抗和高敏CRP、游离脂肪酸(FFA)、血糖、血压、血脂等危险因素的关系。方法选取2009年6月—2010年2月于内分泌科病房治疗的老年2型糖尿病患者82例,根据体质量指数分为糖尿病非肥胖组40例及糖尿病肥胖组42例。选取同期老年健康体检者30例为健康对照组。检测空腹血清抵抗素及相关代谢指标,并进行相关性分析。结果糖尿病肥胖组和非肥胖组抵抗素水平均高于健康对照组,差异有统计学意义(P<0.05,P<0.01);糖尿病肥胖组高于糖尿病非肥胖组,差异有统计学意义(P<0.01)。糖尿病肥胖组游离脂肪酸水平显著高于糖尿病非肥胖组及健康对照组,差异有统计学意义(P均<0.01);多元逐步回归分析显示,抵抗素受HOMA-IR、腰臀比影响较大。结论空腹血清抵抗素水平在老年2型糖尿病患者尤其是伴有肥胖的患者中显著升高,与HOMA-IR、腰臀比呈明显的正相关性,抵抗素可能在胰岛素抵抗、肥胖和糖尿病之间发挥重要作用。

饮食诱导肥胖与肥胖抵抗大鼠抵抗素的表达及与胰岛素抵抗的关系

【目的】研究高脂饮食诱导肥胖及肥胖抵抗大鼠脂肪组织抵抗素表达及其与胰岛素抵抗的关系。【方法】采用幼年SD大鼠,随机分为对照组和高脂组,分别以基础饲料和高脂饲料喂养8周,根据体重筛选出肥胖大鼠和肥胖抵抗大鼠。分别于高脂饲养8周和16周时检测肥胖、肥胖抵抗大鼠抵抗素表达,血清抵抗素、胰岛素、胰岛素敏感指数等指标。【结果】肥胖抵抗大鼠抵抗素表达及胰岛素抵抗程度均显著低于肥胖大鼠。随高脂喂养时间延长,差异更加显著。【结论】肥胖抵抗与肥胖的发生和抵抗素不同程度的表达相关。

血清抵抗素、超敏C反应蛋白与2型糖尿病患者体成分之间的关系

目的观察血清抵抗素及超敏C反应蛋白(hs-CRP)在肥胖、非肥胖2型糖尿病患者中的含量,分析与骨密度(BMD)、体脂成分之间的关系。方法入选病例分3组:正常对照组28例、糖尿病非肥胖组30例、糖尿病肥胖组30例。采用酶联免疫测定法检测空腹血清抵抗素,免疫比浊法测定血清hs-CRP,双能X线骨密度仪(DXA)检测各部位BMD、体内脂肪百分比。通过检测空腹血糖(FPG)与空腹胰岛素(FINS),计算胰岛素分泌功能指数(HOMA2-%B)、胰岛素敏感性指数(HOMA2-%S)以及胰岛素抵抗指数(HOMA2-IR)。结果糖尿病非肥胖组hs-CRP、抵抗素较正常对照组显著升高[(2.34±0.75)mg/L比(1.98±2.24)mg/L;(20.19±11.20)μg/L比(15.59±11.10)μg/L,均P<0.05],糖尿病肥胖组hs-CRP[(4.94±2.35)mg/L]、抵抗素[(25.83±9.56)μg/L]较正常对照组显著升高(P<0.01),亦高于糖尿病非肥胖组(P<0.01)。相关分析显示:抵抗素与BMI存在负相关(r=-0.252,P<0.05),与hs-CRP、HOMA2-%B、HOMA2-IR存在正相关(r分别为0.563、0.225、0.667,均P<0.05),而与各部位BMD无相关性。hs-CRP与腰围(WC)、体重指数(BMI)、HOMA2-IR、上肢脂肪百分比、大腿脂肪百分比、躯干脂肪百分比、全身脂肪百分比存在相关性(r分别为0.773、0.594、0.662、0.540、0.557、0.530、0.561,均P<0.01),与抵抗素、躯干BMD存在相关性(r分别为0.563、0.224,均P<0.05)。校正年龄、空腹血糖等因素之后,hs-CRP仍与WC、BMI、HOMA2-IR、抵抗素和大腿脂肪百分比%独立相关。结论抵抗素与HOMA2-%B、HOMA2-IR相关,表明其在糖尿病发病机制中起重要作用。hs-CRP是已知的炎症因子,hs-CRP与抵抗素的紧密联系提示抵抗素也可能是炎症因子之一。中心性肥胖可能是导致CRP、抵抗素升高的重要原因之一,炎症和(或)肥胖是胰岛素抵抗、2型糖尿病发生的一个启动因子。

抵抗素与胰岛素抵抗及肥胖关系的研究进展

抵抗素是由脂肪组织特异表达分泌的细胞因子.在啮齿类动物实验和离体实验研究显示抵抗素可以诱导机体的胰岛素抵抗,引起糖脂代谢紊乱,和代谢综合征密切相关.但是抵抗素在人体的作用机制尚需更多的研究,另外抵抗素和肥胖的关系也有争议,故本文就抵抗素和胰岛素抵抗及肥胖之间的关系作一综述.