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1.
胰岛素抵抗与高血压 总被引:2,自引:0,他引:2
李光伟 《中华内分泌代谢杂志》1993,9(4):241-242
已有很多研究显示高胰岛素血症、胰岛素抵抗与血压水平密切相关,但在某些肥胖或非胰岛素依赖型糖尿病(NIDDM)人群却未能发现血浆胰岛素水平与血压的正相关关系,尽管这些人群较非肥胖人群有更为明显的高胰岛素血症。值得注意的是即使在胰岛素与血压不相关的材料中也发现胰岛素抵抗与血压水平正相关。为什么会出现这种现象?有些作者认为是胰岛素抵抗而不是高胰岛素血症原发地与高血压相联系,高胰岛素血症是机体对胰岛素抵抗的代偿,高胰岛素血 相似文献
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目的原发性高血压目前被认为是胰岛素抵抗综合征的一部分,我们对老年高血压患者中有关因素进行分析讨论。方法高血压组68人,平均年龄65.7岁,对照组53例,平均年龄63.9岁。测空腹血糖(FBG)、胰岛素(FINS)、血脂4项甘油三酯(TG)。计算体重指数BM I=体重(kg)/身高(m)2、脂肪分布指数WHR=腰围/臀围、胰岛素敏感指数ISI=I/FBG×FINS。结果高血压组的BM I,WHR,FBG,FINS,TG水平高于对照组,ISI低于对照组。经多元分析,ISI与TG,BM I,WHR呈负相关,与HDL呈正相关。结论老年高血压组存在有胰岛素抵抗,这是造成高血压病并发冠心病发生的重要原因之一。 相似文献
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老年人高血压胰岛素抵抗的研究 总被引:1,自引:0,他引:1
本文观察并测定59例老年高血压病患者空腹胰岛素水平和胰岛素敏感指数,发现老年人高血压病级胰岛素水平明显升高,而胰岛敏感指数显著降低,与老年健康对照组比较有显著差异。说明老年高血压患者存在着胰岛素抵抗,并且与靶器官损伤程度和肥胖有关。 相似文献
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研究表明胰岛素抵抗与高血压密切相关,胰岛素抵抗是高血压的一个独立危险因子,二者存在理论上的因果关系.胰岛素抵抗在高血压的发病机制中起至关重要的作用,而高血压也可影响胰岛素的代谢,造成胰岛素抵抗,两者相辅相成,导致一系列严重慢性并发症的发生.同时,多种降压药物可通过影响糖代谢从而改善胰岛素抵抗,另一方面,部分改善胰岛素抵抗的药物可用于治疗原发性高血压.因此,了解胰岛素抵抗与高血 压之间的关系对于胰岛素抵抗及高血压的防治有重要意义. 相似文献
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本文讨论了肥胖、糖脂代谢异常、胰岛素抵抗、高胰岛素血症、细胞内钙离子代谢与高血压之间的相互关系。 相似文献
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上海地区中国人血脂紊乱类型与胰岛素抵抗 总被引:17,自引:0,他引:17
目的:探讨上海地区中国人脂代谢紊乱的类型与胰岛素抵抗的关系。方法:830例年龄≥40岁(男300例,女530例)正常人和血脂紊乱者,后者分为7个亚组,包括单纯低高密度脂蛋白(HDL)组(亚组Ⅰ)、单纯高甘油三酯(TG)组(亚组Ⅱ)、单纯高胆固醇(TC)或高低密度脂蛋白(LDL)组(亚组Ⅲ)、低HDL合并高TG组(亚组Ⅳ)、低HDL合并高TC或高LDL组(亚组Ⅴ)、高TG合并高TC或高LDL组(亚组Ⅵ)、低HDL合并高TG及高TC或高LDL组(亚组Ⅶ),用稳态模式评估法(HOMA)评价胰岛素抵抗(IR)。结果:校正年龄、性别、体重指数等因素后,伴有高TG的各血脂异常 亚组的胰岛素抵抗指数升高较为明显,总体脂、腹部脂肪对血脂紊乱的影响较为显著;体脂对胰岛素抵抗指数的影响部分是通过TG介导的,结论:TG升高可作为个体存在胰岛纱抵抗的指标。 相似文献
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高血压遗传因素与胰岛素抵抗 总被引:11,自引:0,他引:11
目的探讨高血压遗传因素与胰岛素抵抗及其他代谢因素的关系。方法采用家系调查方法,共调查高血压家系25个,包括直系亲属158例,其中高血压54例,血压正常者104例;对照家系15个,直系亲属65人。对比分析高血压家系有无高血压及对照家系直系亲属尿酸、血脂、血糖及胰岛素的差异。结果调整年龄、性别后,在高血压家系中无论是否患高血压,甘油三酯(TG)、TG的对数转换值(logTG)、高密度脂蛋白胆固醇(HDLC)、血浆总胆固醇(TC)/HDLC、尿酸、胰岛素(IN)及其对转换值(logIN)均显著高于对照家系,而高血压家系内有无高血压两组比较,除胰岛素、logIN外,其他因素均无显著差别,进一步调整年龄、性别、体重指数后比较,TG、logTG在三组间差异不再显著,尿酸、TC/HDLC、logIN在高血压家系内高血压及血压正常人群间无显著统计学差别,但两者与对照家系相比均显著升高。结论具有高血压遗传因素者无论是否患高血压均有显著的胰岛素抵抗和代谢紊乱,这些代谢异常可能在超重和高血压发生前就已存在。 相似文献
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高血压大家系中胰岛素抵抗与高血压关系的研究 总被引:9,自引:1,他引:9
目的 探讨胰岛素抵抗是否为所研究高血压大家系的遗传中间表型,研究胰岛素抵抗与高血压关系。方法 我们在北京石景山区收集到一个高血压大家系,共4代约220人,以该高血压大家系成员为观察对象,检测其空腹血糖(FPG),血脂,血浆胰岛素(FINS),计算胰岛素抵抗指数(IR)反映胰岛素抵抗的情况。结果 该家系直系成员高血压组和血压正常组IR值都显著高于家族旁系血压正常(亦无高血压家族史)组。Logistic回归分析显示在家族直系成员中,年龄为影响血压的主要因素,旁系中年龄,IR为影响血压的主要因素,而以IR对血压的影响最大。结论 胰岛素抵抗对该高血压大家系血压水平有一定影响,能否作为其遗传中间表型尚需进一步研究,但在该家系居住的同一地区人群中,胰岛素抵抗是影响血压的重要危险因素,可能同高血压有共同的遗传因素。 相似文献
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胰岛素抵抗与高血压研究的新进展 总被引:1,自引:0,他引:1
本文研究了胰岛素抵抗、高胰岛系血症与高血压的关系,表明前二者参与调节高血压患人群的血压;阐明了胰岛素抵抗、交感神经肾上腺素系统与高血压的关系,即为胰岛素抵抗和高胰岛素血症能刺激交感神经系统,使其活性增加,通过刺激心脏、血管和肾脏引起高血压;并且将抗高血压药物对胰岛素抵抗、交感神经系统活性及脂质代谢的影响问题亦进行了讨论。 相似文献
10.
卡托普利对高血压患者胰岛素抵抗的影响 总被引:6,自引:0,他引:6
测定卡托普利治疗对糖代谢的影响。方法27例高血压(EH)患者卡托普利治疗前及治疗4周后,分别进行口服葡萄糖耐量试验(OGTT),并测定治疗前后的血糖、血浆胰岛素,与20例正常对照组比较。结果两组空腹血糖无明显差异(P>0.05)。EH组OGTT后糖耐量降低(P<0.05),空腹及OGTT后30,60,120,180min血浆胰岛素显著升高(P<0.01),卡托普利治疗后4周,OGTT后60,120min血糖水平较治疗前降低有显著意义(P<0.05)空腹及OGTT血浆胰岛素下降有非常显著意义(P<0.01)。结论EH患者存在高胰岛素血症;卡托普利治疗后,降压的同时胰岛素抵抗也得到某些改善。 相似文献
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Insulin resistance is a characteristic feature of primary hypertension independent of obesity 总被引:26,自引:0,他引:26
The relationship between abnormalities in carbohydrate metabolism and hypertension was studied in 143 newly detected hypertensive patients (59% obese) of both sexes (90 males, 53 females) and compared with 51 normotensive controls. Insulin-mediated glucose disposal assessed with the euglycemic insulin clamp technique was significantly decreased in both non-obese (7.2 +/- 2.1 mg/kg/min; P less than .05) and obese hypertensives (5.1 +/- 2.1 mg/kg/min; P less than .01) compared with the controls (8.4 +/- 1.8 mg/kg/min). The decrease in insulin sensitivity and increase in basal insulin as well as a decreased rate of glucose disposal after an intravenous glucose tolerance test (IVGTT) were verified also after statistical adjustment for sex, age, body mass index, and waist-hip ratio. The insulin index (ratio between peak and basal insulin) during IVGTT was significantly decreased in the hypertensive patients (P less than .001). After the statistical adjustment for the factors mentioned the following lipid abnormalities were still significant: total cholesterol (6.25 +/- 1.12 mmol/L non-obese; 6.06 +/- 1.20 mmol/L obese; 5.41 +/- 1.02 mmol/L controls), triglycerides (1.70 +/- 0.74 mmol/L nonobese; 2.26 +/- 1.13 mmol/L obese; 1.24 +/- 0.53 mmol/L controls) and free fatty acids (0.57 +/- 0.20 mmol/L nonobese; 0.59 +/- 0.20 mmol/L obese; 0.48 +/- 0.15 mmol/L controls). This study shows that after correction for a series of probable confounding variables, hypertension emerges as part of a syndrome characterized by major abnormalities of carbohydrate, insulin, and lipid metabolism, which independently or in concert may act as important risk factors for cardiovascular disease. 相似文献
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We measured the degree of association between obesity, blood pressure, insulin resistance, and insulin secretion in 72 male and female obese hypertensive, obese nonhypertensive, and normal weight control subjects. Baseline weight, body mass index, percent body fat, waist/hip ratio, and systolic and diastolic blood pressures were obtained. Insulin sensitivity was assessed according to Bergman's minimal model. Twelve-hour urinary c-peptide was measured after a standard liquid meal. Insulin action was inversely associated with blood pressure status, obesity status, and age. Meal-stimulated c-peptide excretion significantly correlated with systolic blood pressure and percent fat but not with body mass index or age. Multivariate regression analysis indicated that, of the measures of body composition, percent fat and waist/hip ratio had the strongest correlation with insulin action either alone or in combination with c-peptide excretion. Obese hypertensive patients had an index of insulin action (10(-4).min-1/[microunits/ml]) of 1.34 +/- 0.19, which was significantly (p less than 0.003) lower than in the obese nonhypertensive patients (index, 2.26 +/- 0.10) or the nonobese subjects (index, 5.41 +/- 0.26, p less than 0.001). Meal-stimulated c-peptide excretion (nmol/kg lean body mass) was increased only in the obese hypertensive group (0.32 +/- 0.01) and was significantly higher (p less than 0.001) than in the obese nonhypertensive (0.16 +/- 0.01) or the nonobese subjects (0.14 +/- 0.01). These results support the hypothesis that abnormalities in blood pressure regulation, insulin-stimulated glucose uptake, and insulin secretion coexist. 相似文献
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目的:了解上海社区中老年人超重和肥胖的患病情况以及肥胖相关疾病的患病风险。方法:在上海市嘉定区40岁及以上居民中进行问卷调查、体格检查及生化检测,对其中数据完整的10 375名居民进行统计分析。根据体质量指数(BMI),按照WHO标准界定肥胖和超重者。采用线性回归法分析BMI与一些危险因素的相关性,并采用Logistic回归法分析超重以及肥胖状态对于各种代谢相关性疾病患病风险的影响。结果:本研究人群的BMI均值为25.1±3.3,超重和肥胖的患病率分别为42.92%和7.27%;多元线性回归分析显示:校正多种混杂因素后,随着BMI水平的上升,腰围、收缩压、舒张压、空腹血糖、餐后2 h血糖、总胆固醇、低密度脂蛋白胆固醇、三酰甘油随之增加(均P<0.01),高密度脂蛋白胆固醇随之下降(P 相似文献
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目的 :探讨高血压患者同时存在多种代谢异常时胰岛素的敏感性。方法 :高血压组 79例 ,健康对照组 78例 ,分别进行口服葡萄糖耐量试验 (OGTT)、同步血清胰岛素释放试验 ,血清总胆固醇 (TC)、甘油三酯 (TG)、低密度脂蛋白胆固醇 (L DL- C)、高密度脂蛋白胆固醇 (HDL- C)及体质量指数 (BMI)测定 ,以胰岛素敏感性指数 (ISI)和胰岛素曲线下面积 (IS- AU C)作为胰岛素敏感性的判定指标。结果 :高血压组空腹胰岛素 (FINS)及餐后 2 h胰岛素 (15± 7及 70± 10 m U/L)均显著高于正常对照组 (8± 3及 9± 4 m U/L) ,均为 P<0 .0 1;OGTT显示葡萄糖耐量降低 ,P<0 .0 1。 TC、TG、L DL- C显著升高 ,均 P<0 .0 1,HDL- C升高 ,P<0 .0 5 ;ISI(绝对值 )和 IS- AUC均显著增高 ,分别为 P<0 .0 5与 P<0 .0 1。二组 BMI与 ISI呈显著负相关 ,r分别为 - 0 .4 9,- 0 .37,P<0 .0 5 ;与 FINS呈显著正相关 ,r分别为 0 .5 3,0 .38,P<0 .0 1。结论 :高血压患者存在着高胰岛素血症 ,同时存在着糖代谢及脂蛋白代谢异常。血糖、血脂、体质量指数均影响胰岛素敏感性。 相似文献
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Chiarelli F Marcovecchio ML 《European journal of endocrinology / European Federation of Endocrine Societies》2008,159(Z1):S67-S74
Childhood obesity is a significant health problem that has reached epidemic proportions around the world and is associated with several metabolic and cardiovascular complications. Insulin resistance is a common feature of childhood obesity and is considered to be an important link between adiposity and the associated risk of type 2 diabetes and cardiovascular disease. Insulin resistance is also a key component of the metabolic syndrome, and its prevalence in the paediatric population is increasing, particularly among obese children and adolescents. Several factors are implicated in the pathogenesis of obesity-related insulin resistance, such as increased free fatty acids and many hormones and cytokines released by adipose tissue. Valid and reliable methods are essential to assess the presence and the extent of insulin resistance, the associated risk factors and the effect of pharmacological and lifestyle interventions. The two most common tests to assess insulin resistance are the hyperinsulinemic euglycemic clamp and the frequently sampled i.v. glucose tolerance test utilizing the minimal model. However, both these tests are not easily accomplished, are time consuming, expensive and invasive. Simpler methods to assess insulin resistance based on surrogate markers derived from an oral glucose tolerance test or from fasting insulin and glucose levels have been validated in children and adolescents and widely used. Given the strong association between obesity, insulin resistance and the development of metabolic syndrome and cardiovascular disease, prevention and treatment of childhood obesity appear to be essential to prevent the development of insulin resistance and the associated complications. 相似文献
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吴琪 《China Medical Abstracts (Internal Medicine)》2022,(3):153-154
<正>Objective To establish a more suitable and practicable criterion of metabolically healthy overweight/obesity (MHO/O) in Chinese,a comparison study on different criteria of MHO/O was conducted in subjects aged over 45-year-old in Shanghai Changfeng Community. Method A total of 3301 overweight/obese subjects over 45 years old (men 1 521,women 1 789)in Shanghai Changfeng Community were included in the study. According to the inclusion or exclusion of waist circumference (WC),homeostasis mo... 相似文献
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Insulin resistance in secondary hypertension. 总被引:4,自引:0,他引:4
The insulin sensitivity of five essential hypertensive patients was compared to five patients with renovascular hypertension, five patients with primary hyperaldosteronism, and five normotensive subjects, using the euglycemic hyperinsulinemic clamp technique. Essential hypertensive patients had significantly lower insulin sensitivity than patients with hyperaldosteronism and renovascular hypertensive patients (P = .0066, P = .004, respectively). Hyperaldosteronism patients also had less insulin sensitivity than renovascular hypertensive patients (P = .016). A significant negative correlation was found between body mass index and insulin sensitivity index for essential hypertension patients only (r = -0.87, P less than .003). No such correlation was found in the secondary hypertension patients. The findings suggest a causal relationship between insulin resistance and the development of essential hypertension. Secondary hypertension, on the other hand, is not such an insulin resistant state. 相似文献
19.
Ü. Karaca M.T. SchramA.J.H.M. Houben D.M.J. MurisC.D.A. Stehouwer 《Diabetes research and clinical practice》2014
Impaired microvascular dilatation from any cause and impaired insulin-mediated capillary recruitment in particular result in suboptimal delivery of glucose and insulin to skeletal muscle, and subsequently impairment of glucose disposal (insulin resistance). In addition, microvascular dysfunction, through functional and/or structural arteriolar and capillary drop-out, and arteriolar constriction, increases peripheral resistance and thus blood pressure. Microvascular dysfunction may thus constitute a pathway that links insulin resistance and hypertension. Overweight and obesity may be an important cause of microvascular dysfunction. Mechanisms linking overweight and obesity to microvascular dysfunction include changes in the secretion of adipokines leading to increased levels of free fatty acids and inflammatory mediators, and decreased levels of adiponectin all of which may impair endothelial insulin signaling. Microvascular dysfunction may thus constitute a new treatment target in the prevention of type 2 diabetes mellitus and hypertension. 相似文献
20.
Associations of overweight/obesity and socioeconomic status with hypertension prevalence across racial and ethnic groups
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Deborah Rohm Young PhD Heidi Fischer PhD David Arterburn MD Daniel Bessesen MD Lee Cromwell MS Matthew F. Daley MD Jay Desai PhD Assiamira Ferrara MD PhD Stephanie L. Fitzpatrick PhD Michael A. Horberg MD Corinna Koebnick MSc PhD Claudia L. Nau PhD Caryn Oshiro PhD Beth Waitzfelder Ayae Yamamoto ScM 《Journal of clinical hypertension (Greenwich, Conn.)》2018,20(3):532-540
Racial/ethnic disparities in the prevalence of diagnosed hypertension are persistent but may be partially explained by racial/ethnic differences in weight category and neighborhood socioeconomic status. The authors compared hypertension prevalence rates among 4 060 585 adults with overweight or obesity across 10 healthcare systems by weight category and neighborhood education level in geographically and racially diverse individuals. Data were obtained from electronic health records. Hypertension was defined as at least two outpatient visits or one inpatient hospitalization with a coded diagnosis. Logistic regression, adjusted for age, sex, and site, with two‐way interactions between race/ethnicity and weight category or neighborhood education, was used to examine the association between hypertension and race/ethnicity, with whites as the reference. Results documented that odds ratios for hypertension prevalence were greater for blacks, American Indians/Alaskan Natives, Asians, and Native Hawaiians/other Pacific Islanders compared with whites and lower for Hispanics in similar weight categories and neighborhood education levels. Although two‐way interactions were statistically significant, the magnitude of the odds of hypertension compared with whites did not substantially vary across weight or neighborhood education. Hypertension odds were almost double relative to whites for blacks and Native Hawaiians/other Pacific Islanders across most weight categories and all neighborhood education levels. Odds of hypertension were about 50% greater for Asians relative to whites across weight categories. Results suggest that other factors might be associated with racial/ethnic disparities in hypertension. More research is needed to understand the many factors that may contribute to variation in diagnosed hypertension across racial/ethnic groups with overweight or obesity. 相似文献