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1.
不同糖代谢状态人群胰岛素抵抗和胰岛β细胞功能研究   总被引:16,自引:0,他引:16  
目的探讨从正常糖耐量到糖尿病(DM)不同糖代谢水平,胰岛素抵抗(IR)与胰岛β细胞功能的演变.方法青岛市区30~74岁的正常糖耐量(NGT)447例;空腹血糖受损(IFG)142例;糖耐量受损(IGT)93例;IFG合并IGT(IFG+IGT)42例;新诊DM 153例.采用HOMA-IR评价IR,HOMA-β、ΔI30/ΔG30分别评价基础状态下及糖负荷后的早期胰岛β细胞功能.结果 IFG组HOMA-IR为1.14±0.06,明显高于NGT组的0.93±0.03(P<0.05),IFG组HOMA-β为4.53±0.06,低于NGT组5.10±0.04(P<0.05),两组间△I30/△G30差异无显著性(4.86±0.11 vs 4.99±0.11);IGT组HOMA-IR为1.12±0.07,明显高于NGT(P<0.05),两组间HOMA-β差异无显著性,IGT组△I30/△G30 为4.62±0.14,低于NGT组的4.99±0.11(P<0.05);DM组HOMA-IR为1.55±0.05,明显高于NGT、IGT和IFG组(P<0.05),DM组HOMA-β和△I30/△G30 分别为3.94±0.06、3.93±0.12,明显低于其他各组(P<0.05),DM组基础与糖负荷后的胰岛β细胞功能均明显受损.结论 IFG患者主要表现β细胞功能缺陷,IGT为胰岛素早期分泌受损,DM患者兼有严重的IR和β细胞缺陷.从NGT到DM,随着糖代谢的不断恶化,IR逐渐加重,胰岛β细胞功能进行性减退,最终发生胰岛β细胞功能衰竭.  相似文献   

2.
周燕  苏珂  于健  彭鹰  胡永玲 《山东医药》2006,46(7):11-12
目的探讨2型糖尿病(T2DM)家系正常糖耐量一级亲属(简称一级亲属)血清脂联素、瘦素水平的变化,研究脂联素、瘦素与胰岛素抵抗(IR)的关系。方法收集T2DM家系45个。在排除DM和糖耐量减退的前提下,选择一级亲属为观察组(83例),先证者或其同胞的配偶为正常对照组(76例),检测所有受试者脂联素、瘦素水平,计算胰岛素抵抗指数(HOMA—IR)。结果观察组的脂联素水平显著低于对照组(P〈0.01),HOMA—IR、瘦素显著高于对照组(P〈0.05)。相关分析显示,脂联素与瘦素呈负相关。多元线性逐步回归分析显示,脂联素、瘦素是影响T2DM家系一级亲属IR的独立危险因素。结论T2DM家系一级亲属在未发生DM时已存在IR抵抗,脂联素与瘦素都参与了IR发生过程。  相似文献   

3.
根据口服糖耐量试验将34例沈阳地区研究对象分为正常糖耐量(NGT)组、新生腹血糖受损(新IFG)组、新糖耐量减低(新IGT)组和旧糖耐量减低(旧IGT)组.运用高胰岛素正葡萄糖钳夹技术测定胰岛素抵抗程度,用静脉葡萄糖刺激胰岛素释放试验测定胰岛素一相分泌量和二相分泌量.结果胰岛素钳夹试验NGT、新IFG、新IGT、旧IGT组的葡萄糖输注速率(GIR,mg/kg/min)分别为10.2±0.9;6.0±0.9;58±0.7;44±0.3.新IFG、新IGT、旧IGT组均比NGT组显著减低(P<0.001;P<0.001;P<0.001).胰岛β细胞功能①胰岛素-相分泌量(mU/l)新IFG、新IGT、旧IGT组分别为220±61;331±89;115±18;与NGT组(221±27)相比,新IFG和NGT组处于同一水平,但新IGT有高于NGT组的趋势,而旧IGT组有降低趋势但无统计学差异(P>0.05).②胰岛素二相分泌量(mU/l)NGT、新IFG、新IGT、旧IGT组分别为88±7;110±19;220±80;122±7,新IGT组明显高于其它三组(P<0.01;P<0.05;P<0.05).结论新旧空腹血糖切点划分出的IGR均出现了胰岛素抵抗,胰岛素的分泌模式也和NGT有了差异.  相似文献   

4.
目的 探讨脂联素在不同糖调节受损者冠脉病变发生及严重程度中的临床意义.方法 疑似冠心病行冠脉造影者210例,分为正常血糖组(NGT) 42例,空腹血糖调节受损组(IFG) 36例,糖耐量受损组(IGT)92例(其中IGT1组44例2 h 血糖<10 mmol/L;IGT2组48例2h血糖≥10mmol/L),IFG+IGT组40例.检测体重指数、血压、血脂、胰岛素、脂联素、C反应蛋白,并进行Gensini评分.结果 IGT、IFG+IGT组冠心病患病率及Gensini评分显著高于IFG及NGT(P<0.05);脂联素在IGT、IFG+IGT两组中显著低于IFG、NGT组(P<0.05),C反应蛋白在IGT、IFG+IGT两组显著升高(P<0.05);IGT2组较IGT1组Gensini显著升高、脂联素显著下降(P<0.05);Gensini与脂联素负相关,与C反应蛋白、HOMA-IR正相关(p<0.05);多因素逐步回归分析显示脂联素和HOMA-IR是冠脉病变严重程度独立影响因素.结论 低脂联素血症可更敏感地预测IGR患者的冠脉病变程度,尤其在IGT组中,如餐后血糖控制在10 mmol/L以下可能会带来更大的心血管获益.  相似文献   

5.
目的研究不同血糖水平老年人脂联素、瘦素水平的变化,脂联素瘦素比值与胰岛素抵抗的相关性。方法选取不同血糖水平老年人146例,包括对照组:糖耐量正常的健康人群52例,研究组:糖耐量异常(IGT)患者39例,新近诊断糖尿病(T2DM)患者55例。研究脂联素、瘦素水平以及其比值和胰岛素抵抗指数、体重指数、腰臀比、血脂等指标的相关性。结果 IGT组和T2DM组的腰臀比、体重指数、甘油三酯、瘦素、胰岛素抵抗指数较正常对照组显著增加,脂联素水平较正常组明显下降;脂联素/瘦素与腰围、腰臀比、体重指数、空腹胰岛素、甘油三酯、低密度脂蛋白、HO-MA-IR负相关,与高密度脂蛋白正相关。Logistic回归结果显示脂联素/瘦素是胰岛素抵抗指数的独立危险因素。结论不同血糖水平老年人中,脂联素/瘦素比值与胰岛素抵抗密切相关。  相似文献   

6.
目的 探讨辅助性T细胞1型/2型(Th1/Th2)免疫失衡在中老年IFG发病中的作用及与IR的关系.方法 根据FPG及2hPG将381例中老年糖尿病患者分为IFG1、IFG2、IGT、T2DM、糖耐量正常(NGT)组.ELISA检测血浆干扰素γ(IFN-γ)、白介素-4(IL-4),同时检测胰岛素及HbA1c水平.结果 IFG1、IFG2、IGT组与NGT组比较,胰岛素抵抗指数(HOMA-IR)均增加(P<0.05),但3组间差异无统计学意义(P>0.05).T2DM组与其他组比较,HOMA-IR差异有统计学意义(P<0.05),IFG1、IFG2、IGT、T2DM组胰岛β细胞功能指数(HOMA-β)与NGT组比较均降低(P<0.05),IFG2组与IFG1组比较,IFN-γ升高(P<0.05),IL-4变化差异无统计学意义(P>0.05).结论 中老年IFG人群存在IFN-γ和IL-4升高,HOMA-IR与HOMA-β下降.  相似文献   

7.
胰岛素抵抗(IR)和胰岛素分泌不足是2型糖尿病(T2DM)的重要发病机制,IR是预测T2DM发生的独立危险因素。大量研究发现脂联素、瘦素参与了T2DM IR的发生和发展〔1〕。T2DM患者一级亲属IR程度显著高于无家族史者,脂联素与瘦素联合影响T2DM患者一级亲属的IR程度〔2〕。因此我们测定T2DM正常糖耐量一级亲属(NFDR)血清脂联素、瘦素水平,以进一步探讨NFDR脂联素、瘦素的变化及与IR的关系。1对象与方法1.1对象以T2DM患者NFDR60例为NFDR组,男27例,女33例,年龄38~62(平均42±7)岁,体重指数(BMI)(24.7±3.2)kg/m2,同时选择同期无糖…  相似文献   

8.
目的 探讨2型糖尿病(T2DM)患者血浆内脏脂肪素、瘦素水平与胰岛素抵抗(IR)的相关性.方法 102例T2DM患者和64例正常糖耐量(NGT)对照者,根据BMl分为肥胖组(Ob)和非肥胖(Non-Ob)组,均测定空腹血浆内脏脂肪素、瘦素和相关临床指标,计算胰岛素抵抗指数(HOMA-IR)和腰臀比(WHR).结果 T2DM组与NGT组比较空腹血浆内脏脂肪素和瘦素水平明显升高(t=3.922,P=0.00;t=2.128,P=0.038).相关分析显示T2DM患者空腹血浆内脏脂肪紊与HOMA-IR、WHR、瘦素、HbA<,1> c和TG正相关(r=0.543,P=0.001;r=0.442,P=0.008;r=0.385,P=0.013,r=0.345,P=0.025;r=0.427,P=0.005),瘦素与HOMA-IR、性别、BMI正相关(r=0.578,P<0.01;r=0.547,P<0.01;r=0.607,P<0.01).结论 T2DM患者空腹血浆内脏脂肪素和瘦素水平显著升高,且与IR关系密切.  相似文献   

9.
目的 游离脂肪酸 (FFAs)水平在不同糖代谢状态下对胰岛素抵抗和胰岛 β细胞分泌功能的影响。 方法 选自2 0 0 1- 0 5 2 0 0 3- 11在中国医科大学附属第一医院住院的糖耐量正常 (NGT) 2 8例 ,空腹血糖异常 (IFG)患者 2 0例 ,糖耐量低减 (IGT)患者 2 3例 ,IFG/IGT患者 2 6例 ,2型糖尿病 (T2DM)患者 2 5例。测定各组FFAs水平 ,稳态模型评估胰岛素敏感性 ,HOMA IS及OGTT中糖负荷后 30分钟胰岛素增值与血糖增值的比值评估胰岛 (细胞分泌功能。结果  (1)IGT组、IFG/IGT组及T2DM组患者FFAs水平明显高于NGT组 ;IFG/IGT组患者FFAs水平明显高于IFG组 ;T2DM组患者FFAs水平低于IGT组。 (2 )IGT组、IFG/IGT组及T2DM组患者HOMA IR均明显高于NGT组。(3)胰岛素分泌功能均以T2DM患者变化最显著。 (4)FFAs与HOMA -IR呈正相关 ;FFAs与胰岛素分泌指数呈负相关 ,FFAs与HOMA β细胞功能指数呈负相关。 结论 FFAs水平与胰岛素抵抗和胰岛素分泌缺陷密切相关  相似文献   

10.
目的探讨不同糖耐量者血清超敏C-反应蛋白(hs-CRP)的表达及与胰岛素抵抗的相关性。方法对2004年10月至2005年4月中国医科大学附属第一医院体检中心90名体检者(男53名,女37名),根据标准75g口服葡萄糖耐量试验(OGTT)分为正常糖耐量(NGT)组、单纯空腹血糖受损(IFG)组、单纯糖耐量异常(IGT)组、同时合并IFG/IGT组及2型糖尿病(T2DM)组,采用酶联免疫吸附(ELISA)法分别检测各组血清hs-CRP,并与稳态模型胰岛素抵抗指数(HOMA-IR)作相关分析。结果IFG组、IFG/IGT组及T2DM组hs-CRP均明显高于NGT组,并与糖代谢指标及HOMA-IR呈正相关。结论T2DM患者早在IFG阶段就已经存在炎症状态,炎症可能参与了T2DM的发生与发展。  相似文献   

11.
BACKGROUND: The lipid-lowering drug niacin has attracted renewed interest because it raises HDL-cholesterol and because it has recently been found to slow down the progression of intima media thickness in patients with coronary heart disease. Since niacin acts on adipocytes, we investigated its impact on adipokines and on some functions attributed to adipokines. METHODS AND RESULTS: In a randomized, placebo-controlled, double-blind study 30 men with the metabolic syndrome were treated for 6 weeks with 1500 mg extended-release niacin (n=20) or a placebo (n=10). Adiponectin increased by 56% (p<0.001) and leptin by 26.8% (p<0.012). Resistin, TNF-alpha, IL-6, and high sensitive CRP remained unchanged. In spite of the increase in adiponectin there was no improvement in endothelial function. The HOMA index actually deteriorated by 42% (p<0.014). CONCLUSION: Short-term treatment with extended-release niacin causes a pronounced increase in adiponectin but fails to improve atheroprotective functions attributed to adiponectin, such as insulin sensitivity, anti-inflammation and endothelial function.  相似文献   

12.
Heat stress (HS) induces adaptive responses that are responsible for alterations of carbohydrate and lipid metabolism. This study aimed to evaluate the effects of chronic heat treatment on the expression and secretion of leptin and adiponectin, important regulators of energy homeostasis, food intake and insulin action. C57BL/6 mice were subdivided into three groups (24 mice each). The first group was kept under control conditions (C: 22±2?°C). The second group was exposed to HS (35±1?°C). The third group was kept under control conditions and was food restricted (FR). The HS group had higher rectal temperature than the C and FR groups and lower food intake than the C group. Hspa1 (Hspa1a) gene expression in adipose tissue, muscle and liver was higher under HS than FR and C. Heat treatment resulted in decreased blood glucose and non-esterified fatty acids; increased leptin, adiponectin and insulin secretion; and greater glucose disposal. Leptin, adiponectin, leptin and adiponectin receptors, insulin receptor substrate-1 and glucose transporter mRNAs were up-regulated in HS mice. This study provides evidence that HS improves leptin and adiponectin signalling in adipose tissue, muscle and liver. Heat stress was responsible for improving insulin sensitivity and glucose uptake in peripheral tissues, probably mediated by adipokines. Changes in the adipokine levels and sensitivity to them may be considered as an adaptive response to heat.  相似文献   

13.
瘦素、脂联素与高血压的相关性   总被引:5,自引:0,他引:5  
尽管瘦素和脂联素都由脂肪组织分泌,但是高血压患者的瘦素水平升高[1],而脂联素水平降低[2],这说明二者在高血压的发生及发展中既有联系又有区别,本文就瘦素、脂联素生物学特性及其与高血压的关系的研究进展进行综述。瘦素的生物学结构与作用1.瘦素的生物学结构:瘦素是一种主要  相似文献   

14.
Lipodystrophies are characterized by selective but variable loss of body fat and metabolic complications of insulin resistance. We hypothesized that reduced synthesis and secretion of adipocyte-specific proteins may be related to the metabolic complications of lipodystrophy. Therefore, we compared fasting serum concentrations of adiponectin and leptin, in 18 patients with congenital generalized lipodystrophy (CGL), 11 with acquired generalized lipodystrophy (AGL), 46 with familial partial lipodystrophy-Dunnigan variety (FPLD) and 18 with acquired partial lipodystrophy (APL) and studied their relationship to metabolic parameters. Patients with CGL and AGL had markedly reduced serum adiponectin levels compared to those with FPLD and APL (median [range]: 1.5 [0.4-7.5], 3.2 [0.6-7.7], 6.9 [1.9-23.2] and 7.9 [3.1-13.3] microg/mL, respectively, p < 0.0001); the same trend was noted for serum leptin levels (0.63 [0.05-3.7], 2.18 [0.05-11.30], 2.86 [0.23-9.00] and 6.24 [1.21-10.4] ng/mL, respectively, p < 0.0001). Serum adiponectin levels correlated negatively with fasting serum triglycerides (r = -0.6, p < 0.001) and insulin levels (r = -0.5, p < 0.0001) and positively with serum high-density lipoprotein cholesterol levels (r = 0.5, p < 0.001). Serum adiponectin levels were lower in patients with diabetes compared to non-diabetic subjects (3.0 vs. 7.1 microg/mL, p < 0.001). Our results indicate that serum adiponectin and leptin levels are extremely low in patients with generalized lipodystrophies and may be related to severe insulin resistance and its metabolic complications in lipodystrophies.  相似文献   

15.
OBJECTIVE: The study was designed to examine the effect of percutaneous coronary intervention (PCI) on adiponectin and leptin levels. We have previously demonstrated that PCI triggers a systemic inflammatory response. We hypothesized that inflammation participates in the pathogenesis of diabetes mellitus and the metabolic syndrome by modulating levels of adiponectin and leptin. DESIGN: Prospective study in which inflammation was induced by PCI. PATIENTS: Forty-eight patients with stable coronary artery disease and without diabetes mellitus. MEASUREMENTS: High-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), leptin and adiponectin were measured at baseline and 48 h after the procedure. RESULTS: Following PCI, hs-CRP increased by 211%, IL-6 by 87% and leptin by 19%, while adiponectin decreased by 14% (P < 0.001 for all). The change in IL-6 correlated with that in hs-CRP (rho = 0.32; P = 0.027), as did the changes in IL-6 and leptin (rho = 0.31; P = 0.03). The change in adiponectin, however, did not correlate with the change in any of the other markers. CONCLUSION: This study demonstrates that PCI affects the levels of adiponectin and leptin within 48 h. These effects may be secondary to the inflammatory response triggered by PCI.  相似文献   

16.
Regulation of T cell-mediated hepatic inflammation by adiponectin and leptin   总被引:10,自引:0,他引:10  
Concanavalin A-induced hepatotoxicity was compared in lipodystrophic aP2-nSREBP-1c transgenic mice (LD mice) lacking adipose tissue, obese leptin-deficient ob/ob mice, and lean wild-type (WT) mice. Serum leptin and adiponectin were low in LD mice, whereas ob/ob mice had undetectable leptin, but high adiponectin. Protection from hepatotoxicity was observed in ob/ob, but not in LD mice, despite low cytokine levels and reduced T cell activation and hepatic natural killer T cells in both groups. Administration of adiponectin protected LD mice from hepatotoxicity without altering cytokine levels. In contrast, administration of leptin heightened disease susceptibility by restoring cytokine production. Neutralization of TNF alpha protected LD mice from liver damage. Increased in vivo susceptibility to the hepatotoxic effect of TNF alpha was observed in LD mice. In vitro, adiponectin protected primary hepatocytes from TNF alpha-induced death, whereas leptin had no protective effect. In conclusion, although leptin increases susceptibility to hepatotoxicity by regulating cytokine production and T cell activation, adiponectin protects hepatocytes from TNF alpha-induced death.  相似文献   

17.
Objective  Rett syndrome is a progressive neurological disorder affecting almost exclusively females after age 6 months and characterised by acquired microcephaly, psychomotor retardation, growth failure, purposeless hand movements, autistic-like behaviour and wide-based and stiff legged gait. Leptin and adiponectin, peptides secreted by adipose tissue, are involved in the regulation of body weight and energy expenditure.
Design and patients  We investigated in patients with Rett syndrome the variations of plasma leptin and adiponectin and their relation over a 2-year period. Sixteen female patients, mean age at the basal time 9·4 ± 4·3 years, with classical Rett syndrome were enrolled. Controls were 16 healthy female subjects, mean age at the basal time 9·9 ± 3·4 years.
Measurements  Blood samples were withdrawn in the morning at the baseline, 12 months after and 24 months after; plasma leptin and adiponectin concentrations were detected by ELISA.
Results  In patients, leptin concentrations significantly increased, while adiponectin concentrations significantly decreased. Both leptin and adiponectin values were significantly higher than those found in controls at each time. Leptin significantly correlated with adiponectin in patients, while there was not a significant correlation in controls.
Conclusion  Since all patients were not obese, we might hypothesize that in Rett syndrome leptin and adiponectin might participate to clinical manifestations other than weight balance.  相似文献   

18.
瘦素、脂联素是新发现的重要脂肪因子.近年来瘦素、脂联素在NAFLD、丙肝及肝硬化等慢性肝病中的作用已引起众多学者的关注,多数研究发现在非酒精性脂肪肝和丙肝患者中血清瘦素水平增高而脂联素水平降低,而这些脂肪因子在慢性肝痛发生发展中的作用还未完全阐明,各家报道不一.本文就瘦素、脂联素与慢性肝病的研究进展作一综述.  相似文献   

19.
Primary hyperparathyroidism (PHPT) has been associated with high cardiovascular morbidity and mortality; its pathogenesis is not fully understood. Moreover, many metabolic abnormalities are frequently present in patients with PHPT. Several substances (such as leptin and adiponectin) are secreted from adipocytes, which may contribute to regulate energy homeostasis and the development of cardiovascular diseases. We examined the relationship between leptin and adiponectin levels and metabolic disorders in 67 newly diagnosed never-treated patients with PHPT and in 46 healthy subjects (HS). Twenty (29.8%) patients with PHPT presented a metabolic syndrome (as defined by Adult Treatment Panel III criteria). Serum leptin and adiponectin levels in HS were 6.28 +/- 3.3 ng/mL (range, 1.7-19.2 ng/mL) and 6.65 +/- 1.7 microg/mL (range, 3.72-10.86 microg/mL), respectively. In all patients with PHPT, the mean leptin levels (34.28 +/- 20.4 ng/mL) were significantly higher than those of HS (P < .01) and, in particular, in PHPT patients with metabolic syndrome (52.63 +/- 31.2 ng/mL) and positively correlated with body mass index, waist circumference, and cholesterol. The mean adiponectin level was significantly lower (4.34 +/- 3.5 mug/mL) only in PHPT patients with metabolic syndrome (P < .005) and negatively correlated with waist circumference and fasting glucose. We concluded that increased serum level of leptin and decreased serum level of adiponectin coexist in patients with PHPT and may represent a pathogenetic factor for cardiovascular disease in this condition.  相似文献   

20.
The evolving role of leptin and adiponectin in chronic liver diseases   总被引:9,自引:0,他引:9  
Leptin and adiponectin, the main metabolic products of adipose tissue, have been implicated in a wide spectrum of human diseases. Given the frequent presence of hepatic steatosis in several chronic liver diseases, there is currently increasing interest in the role of these adipokines in the development of hepatic steatosis and also in necroinflammation and fibrosis, mostly in patients with nonalcoholic fatty liver disease or chronic hepatitis C. According to experimental data, reduced adiponectin levels and increased leptin levels associated with leptin resistance, which are usually observed in obese patients with or without metabolic syndrome, may result in fat accumulation in the liver and in the enhancement of liver inflammation and mostly fibrogenesis. Increased leptin and decreased adiponectin serum levels have been detected initially in patients with nonalcoholic steatohepatitis and more recently in patients with chronic hepatitis C compared to healthy controls in most but not all studies, while the data on the associations between these adipokine levels and the severity of hepatic steatosis or fibrosis are still rather conflicting. However, several potential confounding parameters were not evaluated in all studies. Therefore, the associations between adipokines and liver histological lesions and their effects on liver cells should be evaluated further in prospective, carefully designed studies, including larger cohorts of patients with detailed assessment of metabolic and other potential confounding factors.  相似文献   

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