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1.
目的 探讨妊娠期糖尿病(GDM)患者血清脂联素和肿瘤坏死因子α(TNF-α)水平与胰岛素抵抗(IR)关系.方法 检测48例GDM患者(GDM组)、30例正常葡萄糖耐量妊娠者(NGT组)血清脂联素、TNF-α,分析两者与IR指数的相关性.结果 与NGT组比较,GDM组血清脂联素水平下降(P<0.01),TNF-α升高(P<0.01).脂联素与IR呈负相关(P<0.01),TNF-α与IR呈正相关(P<0.01).体质量指数(BMI)、脂联素和TNF-α是影响GDM患者IR的独立危险因素.结论 GDM患者血清低脂联素水平、高TNF-α水平与IR密切相关,是GDM发生发展的重要影响因素.  相似文献   

2.
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。  相似文献   

3.
初发2型糖尿病患者血脂联素和瘦素与胰岛素抵抗的关系   总被引:1,自引:0,他引:1  
目的 研究初发2型糖尿病患者血脂联素和瘦素水平的变化及其与胰岛素抵抗的关系.方法 选择46例初发2型糖尿病患者,及与其体脂含量相匹配的糖耐量正常者43名,计算体重指数(BMI)和腰臀围比(WHR),并空腹采血,测定血糖(FPG)、血脂、真胰岛素(FTI)、胰岛素原(FPI)、脂联素和瘦素浓度,分析血清脂联素和瘦素水平的变化及其与胰岛素抵抗的关系.用胰岛素抵抗指数(HOMA-IR)评估胰岛素抵抗程度.结果 2型糖尿病组与正常对照组比较,年龄、BMI无统计学意义(P>0.05),三酰甘油、FPG及FPI和HOMA-IR明显升高(P<0.05或P<0.01),舒张压、脂联素水平明显降低(P<0.05或P<0.01);相关分析显示,脂联素与FPG、FTI、HOMA-IR、BMI、WHR呈负相关(P<0.05或P<0.01);瘦素与BMI、FTI、HOMA-IR、FPG呈正相关(P<0.05或P<0.01),与WHR无关.人血清脂联素和瘦素间无相关性.结论 人血清脂联素和瘦素与胰岛素抵抗密切相关,体脂含量相同的初发2型糖尿病患者血脂联素水平低于正常人.  相似文献   

4.
目的 探讨2型糖尿病患者血清脂联素、瘦素及二者比值与冠状动脉病变的关系.方法 对行冠状动脉造影的180例2型糖尿病患者的大血管病变危险因素进行采集,分为冠心病组和对照组,冠心病组又分为单支病变组、双支病变组和多支病变组,测量脂联素和瘦素的变化,分析脂联素/瘦素比值与冠状动脉病变的关系.结果 与对照组比较,冠心病组总胆固醇、纤维蛋白原定量和空腹血C反应蛋白升高,高密度脂蛋白胆固醇、脂联素和脂联素/瘦素比值(2.78比1.16)降低.相关分析表明,冠心病组中冠状动脉狭窄程度与年龄、纤维蛋白原定量和C反应蛋白呈正相关,与脂联素和脂联素/瘦素比值(r=-0.314)呈负相关.在校正体质指数后,冠状动脉狭窄程度与脂联素/瘦素比值仍呈负相关(r=-0.541).多因素Logistic回归分析显示,脂联素/瘦素比值降低是冠状动脉病变的危险因素.脂联素/瘦素比值随冠状动脉病变支数增加而变小(2.10比1.37比 0.72 ),组间差异有统计学意义.分层结果显示,当冠状动脉病变支数逐渐升高时,脂联素/瘦素比值与冠状动脉危险因素仍然相关,而稳态胰岛素评估模型胰岛素抵抗与冠状动脉危险因素不再相关.结论 2型糖尿病患者中,脂联素/瘦素比值降低与动脉粥样硬化的形成有关.脂联素/瘦素比值可望作为评估动脉粥样硬化程度的血清学标志.脂联素/瘦素比值相对于稳态胰岛素评估模型胰岛素抵抗是一个较好评估胰岛素抵抗致冠状动脉病变的指标.  相似文献   

5.
妊娠糖尿病患者血清瘦素水平与胰岛素抵抗的关系   总被引:4,自引:0,他引:4  
28例妊娠糖尿病(GDM)患者和30例正常对照组(NGT)的研究显示,GDM组瘦素、空腹胰岛素、甘油三酯和胰岛素抵抗指数水平均比NGT组显著升高;瘦素和孕前BMI是影响GDM患者胰岛素抵抗的独立危险因子。  相似文献   

6.
腺苷酸活化蛋白激酶(AMPK)作为细胞重要的能量感受器,能通过增强分解代谢通路,抑制合成代谢通路,调节代谢和能量平衡.近年来研究显示AMPK同样参与了以瘦素、脂联素及抵抗素等为代表的脂肪细胞因子生理作用的发挥,同时AMPK激活亦可影响脂肪细胞因子的分泌,因此脂肪细胞因子与AMPK相关作用机制的研究将为治疗肥胖、糖尿病和代谢综合征提供新的途径.  相似文献   

7.
目的测定2型糖尿病(T2DM)患者及其非糖尿病一级亲属(FDRs)血清游离脂肪酸(FFA)、脂联素水平,评估其胰岛素敏感性,分析FFA、脂联素与胰岛素抵抗(IR)之间的关系。方法测定健康对照组(46例)、FDRs组(43例)和T2DM组(30例)的血清FFA及脂联素,用IR指数(HOMA-IR)评估胰岛素敏感性,分析各指标在3组之间的差异及相关性。结果FFA在对照组(0.36±0.14)mmol/L、FDRs组(0.52±0.17)mmol/L和T2DM组(0.68±0.23)mmol/L,呈依次增高趋势,差异有统计学意义(P〈0.05)。脂联素在对照组和FDRs组分别为(10.25±2.34)mg/L和(6.03±1.91)mg/L,差异有统计学意义(P〈0.01);而T2DM组为(4.75±1.27)mg/L,低于FDRs组,差异有统计学意义(P〈0.01);HOMA-IR在对照组、FDRs组和T2DM组呈依次增高趋势,差异有统计学意义(P〈0.05)。FFA与HOMA-IR呈正相关,与脂联素呈负相关;脂联素与体质指数、HOMA-IR呈负相关。结论FDRs组已经存在IR,并且血清FFA水平升高,脂联素水平降低;FFA、脂联素与IR密切相关,可作为评估IR的较好指标。  相似文献   

8.
非酒精性脂肪肝患者胰岛素抵抗与脂联素基因表达的关系   总被引:1,自引:0,他引:1  
目的探讨NAFLD患者胰岛素抵抗(IR)与脂肪组织脂联素基因表达的关系。方法用SYBR GreenI实时定量RT-PCR方法检测脂肪组织脂联素mRNA的表达水平,用稳态模型法计算IR指数。结果肥胖和非肥胖NAFLD患者及对照组IR指数分别为:3.0±0.8、2.8±0.9和2.0±0.6、1.2±0.5,其脂肪组织脂联素基因表达和血浆脂联素浓度较对照各组显著降低(P〈0.05),IR与脂联素基因表达(r=0.5,P〈0.05)和血浆脂联素浓度负相关(,=0.4,P〈0.05),与血清甘油三酯正相关(r=0.3,P〈0.05)。结论NAFLD患者的IR与脂肪组织脂联素基因低表达有关,脂联素基因低表达在IR和NAFLD发病中起了一定作用。  相似文献   

9.
<正>传统上,普遍认为脂肪组织为能源仓库,由于肥胖和代谢疾病发病率的迅速增加,脂肪组织也获得了巨大的研究价值,其分泌的脂肪因子除了调节脂肪存储和养分平衡,还参与了胰岛素抵抗(IR)、糖脂代谢、炎症调节等病理生理过程。21世纪,糖尿病已成为一种世界范围内的流行病,而其大血管并发症,即动脉粥样硬化所致的心脑血管疾病,是造成患者死亡的主要原因。本文旨在对糖尿病动脉粥样硬化作用较突出的部分脂肪因子作一综述,以阐述其对该病理过程的影响。  相似文献   

10.
目的观察罗格列酮(RSG)对2型糖尿病(T2DM)患者血清脂肪细胞因子的影响,探讨血清脂肪细胞因子和胰岛素抵抗(IR)的关系及其在T2DM发病机制中的作用。方法38例新诊断T2DM患者(DM组),以RSG每日4mg口服治疗12周;24例年龄和性别匹配的糖耐量正常者为正常对照(NC)组。检测NC组及DM组患者治疗前后的身高、体重、血压、FPG、2hPG、免疫反应胰岛素(IRI)、真胰岛素(TI)、胰岛素原(PI)、血清脂肪细胞因子瘦素(LEP)、抵抗素(RST)、脂联素(APN)、视黄醇结合蛋白4(RBP-4)、尿白蛋白(UAlb)和血脂谱。计算BMI、胰岛素敏感性指数(QUICKI)、胰岛素抵抗指数(HOMA-IR)和FPI/FTI。结果DM组RSG治疗前PG、IRI、FPI、LEP、RST、RBP-4、HOMA-IR和FPI/FTI均较NC组升高,而APN和QUICK下降(P〈0.05);DM组RSG治疗后,BMI、UAlb、血脂谱和RBP-4无显著变化,其余指标均向正常转化,APN则升高达2倍多(P〈0.01)。LEP与性别、BMI、FIRI、FTI、FPI、HOMA-IR和QUICKI相关;RST与FPI/FTI和TI相关;APN与年龄、BMI、RBP-4、FPI、2hPI、FTI、HOMA-IR和QuICKI相关;RBP-4与BMI、APN、HOMA-IR相关。多元逐步回归分析提示,LEP和APN与IR独立相关。结论新诊断T2DM患者存在IR和血清LEP、RST、RBP-4升高;APN下降;RSG可能通过改善血清脂肪细胞因子谱而发挥降血糖、改善IR和口细胞功能的疗效。  相似文献   

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目的 探讨瘦素及可溶性瘦素受体(sLR)在妊娠糖尿病发病及胎儿发育中的作用.方法 选取2014年1月至12月在厦门大学附属成功医院连续产检并分娩的673名孕妇为研究对象,跟踪随访至孕晚期.根据糖耐量试验结果,采用随机抽样法选取50例血糖控制良好的妊娠糖尿病患者纳入妊娠糖尿病组,根据一般资料进行匹配选取50名糖耐量试验结果阴性者纳入正常妊娠组.根据妊娠周数分为孕早期和孕晚期亚组,比较两组不同孕期血清及脐血瘦素、sLR、脂联素、抵抗素及生化指标水平,计算稳态模型评估-胰岛素抵抗指数(HOMA-IR),精确测量新生儿生长发育指标,使用多元Logistic回归分析孕早期胰岛素抵抗的危险因素,同时采用Spearman相关性分析血清瘦素与sLR、脂联素、抵抗素及生化指标水平的相关性.结果 与正常妊娠组相比,妊娠糖尿病组孕早期血清瘦素、甘油三酯、总胆固醇、低密度脂蛋白-胆固醇(LDL-C)、空腹胰岛素(FINS)、HOMA-IR明显升高(t=0.938~6.864,P均<0.05),sLR、脂联素显著降低(t=9.237、2.216,P均<0.05),抵抗素、高密度脂蛋白-胆固醇(HDL-C)、空腹血糖差异无统计学意义(P均>0.05).与正常妊娠组相比,妊娠糖尿病组孕晚期血清瘦素、抵抗素、空腹血糖、FINS、甘油三酯、总胆固醇、LDL-C、HOMA-IR明显升高(t=0.429 ~ 13.787,P均<0.05),sLR、脂联素显著降低(t=2.216、5.623,P均<0.05),HDL-C差异无统计学意义(P>0.05).与正常妊娠组相比,妊娠糖尿病组脐血瘦素、抵抗素明显升高(t=1.007、11.857,P均<0.05),sLR、脂联素显著降低(t=0.201、4.558,P均<0.05).多元Logistic回归分析显示,瘦素(OR =1.288,95% CI:1.137 ~4.370)、抵抗素(OR=1.223,95%CI:1.035~ 1.570)、总胆固醇(OR=1.216,95%CI:1.026 ~1.823)、甘油三酯(OR=1.357,95%CI:1.008~ 3.572)、LDL-C (OR=1.634,95% CI:1.251~3.764)是妊娠糖尿病组孕早期发生胰岛素抵抗的独立危险因素,sLR (OR =0.714,95% CI:0.161~0.893)、脂联素(OR =0.352,95%CI:0.112 ~0.510)是妊娠糖尿病组孕早期发生胰岛素抵抗的保护性因素.妊娠糖尿病组孕晚期母体血瘦素含量与sLR、脂联素均呈负相关(r=-0.16、-1.13,P均=0.000),与抵抗素呈正相关(r=0.269,P=0.019).妊娠糖尿病组脐血瘦素含量与sLR、脂联素均呈负相关(r=-0.147、-1.250,P均=0.000),与抵抗素、体重、Ponderal 指数均呈正相关(r =0.410、0.673、0.301,P均<0.05),与头围、身长无关(P均>0.05).结论 瘦素及sLR与妊娠糖尿病患者胰岛素抵抗存在相关性,但与胎儿宫内生长和发育无关.  相似文献   

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Summary Plasma insulin responses and insulin resistance were determined in 75 subjects, defined as having a normal, borderline abnormal, or abnormal oral glucose tolerance test (OGTT). Although considerable heterogeneity of insulin response existed, most patients with abnormal OGTT's had insulin responses greater than normal; none had insulin responses less than normal. The degree of insulin resistance also varied, but most patients with abnormal OGTT's were also abnormally insulin resistant. A significant correlation (r=0.64, p ±0.001) existed between insulin response and the degree of insulin resistance. However, when both variables were taken into consideration, the entire population could be divided into two groups. One group was characterized by both normal insulin responsiveness and sensitivity, the other by increased insulin response, associated with greater insulin resistance. Most patients with abnormal OGTT's fell into the latter group, but some had glucose intolerance without either an exaggerated insulin response or insulin resistance. These results suggest that true heterogeneity exists in patients with abnormal OGTT's.This work was supported in part by grants from the National Institutes of Health, #HL 08506 from the National Heart and Lung Institute and #RR-70 from the General Clinical Research Centers Branch, and from the Research Services of the Veterans AdministrationDr. Reaven is a Medical Investigator, Veterans AdministrationDr. Olefsky is a Clinical Investigator, Veterans Administration  相似文献   

15.
目的了解脂肪肝患者血清瘦素水平变化,探讨其可能的临床意义。方法测定脂肪肝患者肝功、血脂、血糖及胰岛素、血清瘦素水平,测量其身高、体重,计算体重指数、体脂肪含量。瘦素、胰岛素分别采用ELISA、IRA方法测定,胰岛素抵抗用HOMA模式估算。结果脂肪肝组血清瘦素水平高于对照组,与BM I、?t、ALT、CHE相关,与IR无关。结论血清瘦素是脂肪肝患者发病的一个危险因素,与胰岛素抵抗无直接相关性。  相似文献   

16.
Atherosclerosis in diabetes and insulin resistance   总被引:1,自引:0,他引:1  
Atherosclerosis and cardiovascular disease are the major causes of morbidity and mortality in patients with diabetes and those with insulin resistance and the metabolic syndrome. Both conditions profoundly accelerate the development of atherosclerosis and increase the morbidity and mortality of cardiovascular events. The question, therefore, is what are the molecular/biochemical mechanisms that underlie the potentiating influence of diabetes, the metabolic syndrome and/or insulin resistance on the development and progression of atherosclerosis? The following review will focus on the molecular mechanism whereby hyperglycaemia and/or hyperinsulinemia either directly or indirectly promote atherosclerosis.  相似文献   

17.
目的 探讨瘦素在肝硬化发生、发展中的作用.方法 对44例肝硬化患者(肝硬化组)和17例健康查体者(正常对照组)进行血清瘦素、空腹血糖(FPG)、胰岛素(FINS)水平测定并分析相关因素.结果 肝硬化组血清瘦素水平显著高于对照组(P<0.01),肝功能Child-pugh B、C级者显著多于A级(P<0.05);血清瘦素水平与FINS、FPG、胰岛素敏感指数(ISI)呈显著正相关,FINS是瘦素的显著预测因子.结论 肝硬化患者瘦素水平显著升高;其可能通过胰岛素抵抗诱发肝性糖尿病.  相似文献   

18.
Relative hypoleptinaemia in women with mild gestational diabetes mellitus.   总被引:2,自引:0,他引:2  
AIMS: There is increasing evidence suggesting that leptin plays a major role in the regulation of energy homeostasis, as well as in the neuroendocrine and reproductive systems. Leptin is synthesized in the human placenta. The aim of this study was to relate serum leptin levels during pregnancy to glucose tolerance, body mass index (BMI) and specific metabolic variables, such as specific insulin and proinsulin. METHODS: A 2-h 75 g oral glucose tolerance test was performed in 221 pregnant women at 22-29 weeks of gestation (median 25th week). Serum leptin was measured using a radioimmunoassay. In 49 women, sequential leptin measurements were performed (during pregnancy and post partum (median 5 months)). RESULTS: During pregnancy serum leptin was significantly related to body weight (r = 0.49), BMI (r = 0.51), fasting immunoreactive insulin (r = 0.46), specific insulin (r = 0.43) and proinsulin (r = 0.29) (all P-values <0.0001). In women with mild gestational diabetes (GDM, n = 55), leptin levels were lower compared to women with normal glucose tolerance (n = 166) after adjusting for BMI and fasting insulin (26.9 vs. 19.4 ng/ml, P = 0.0001). Leptin was significantly higher during pregnancy compared to post partum (mean +/- SE: 24.3+/-1.5 vs. 19.6+/-1.6 ng/ml, P = 0.0003), even after adjustment for changes in BMI and changes in fasting insulin (P = 0.013). CONCLUSIONS: Leptin levels are elevated in pregnancy. Women with mild GDM presented with relative hypoleptinaemia compared to women with normal glucose tolerance.  相似文献   

19.
Aims To examine the prevalence of gestational diabetes in third‐trimester pregnant women as well as to assess their insulin secretion and insulin resistance (IR). Methods Third‐trimester pregnant women (n = 262) attending antenatal care at local clinics in the central region of the Limpopo Province underwent a 2‐h oral glucose tolerance test (OGTT) with blood collected at 0, 30 and 120 min. Glucose and insulin were measured. Results The prevalence of gestational impaired glucose tolerance (GIGT) and gestational diabetes mellitus (GDM) was 8.8% (7.3% GIGT; 1.5% GDM). Women with GIGT/GDM were significantly older and had more children compared with women with a normal response to the OGTT. Homeostasis model assessment (HOMA)‐IR and fasting insulin were lower in the GIGT/GDM group compared with the normal group, as were measures of insulin secretion (HOMA B‐cell function and insulinogenic index). Furthermore, women with body mass index (BMI) ≥ 30.0 kg/m2 were significantly older and had higher parity, systolic and diastolic blood pressure measurements than those with BMI 25.0–29.9 kg/m2 and BMI < 25.0 kg/m2. However, increased BMI was not associated with an increased risk of GIGT/GDM. Conclusion The present study shows that there is a high prevalence of GIGT/GDM, with most women having IGT. The GIGT/GDM present in these women is characterized by increased insulin sensitivity accompanied by reduced pancreatic B‐cell function. Additionally, heavier women appear to have increased first phase insulin secretion, suggesting the presence of insulin resistance.  相似文献   

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