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代谢综合征定义与胰岛素抵抗 总被引:3,自引:0,他引:3
代谢综合征(metabolic syndrome,MS)已逐渐成为一种临床和公共卫生共同面临的危机,其发病率已达到流行病的规模。其主要临床后果是增加心血管事件(CVD)与糖尿病(DM)的发生,由其引发的全球 相似文献
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巨噬细胞,包括中性粒细胞和树突状细胞,因为其特有的吞噬能力被认为是体内主要的固有免疫效应细胞。近年研究表明巨噬细胞在维持机体代谢平衡的过程中也起着重要作用,它们广泛存在于各种组织,对代谢信号做出应答、产生抗炎因子及其前体因子,从而对代谢过程进行调节。这些充分表明,由于营养过剩引起的代谢应激会使巨噬细胞和免疫系统调节失衡,并且恶性循环,最终导致炎症不可控制,产生代谢紊乱,比如胰岛素抵抗、脂肪肝、动脉粥样硬化与高脂血症等。 相似文献
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目的探讨代谢综合征患者颈动脉内中膜厚度与IR的相关性。方法入选研究对象共90例,分为代谢综合征(MS)组和健康对照组,应用血管彩色超声检测颈动脉内中膜厚度。测量血压、身高、体质量、腰围和臀围。抽取空腹静脉血,测定血清胰岛素(FINS)、血糖(FPG)、总胆固醇(TC)、三酰甘油(TG)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、载脂蛋白AⅠ(Apo-AⅠ)和载脂蛋白B(Apo-B)。结果MS组IMT、IR水平高于健康对照组(P<0.05)。Pearson相关分析显示,IMT与IR、SBP、DBP、WC、WHR、BMI、BF%、FPG、TC均呈显著正相关(P<0.01)。多元逐步线性回归分析显示:收缩压、腰围、IR、血糖是影响IMT的独立因素;IMT、舒张压、HDL-C是影响IR的独立因素。结论代谢综合征患者IMT与IR、收缩压、腰围、血糖密切相关。 相似文献
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目的探讨非酒精性脂肪肝(NAFL)脂代谢紊乱、胰岛素抵抗的情况及其与代谢综合征的关系.方法对284例NAFL患者测体重指数、血压、空腹血糖、胰岛素、肝功、血脂和血尿酸.以96例非脂肪肝的体检者为对照组.两组间年龄和性别构成差异无显著性.结果NAFL组体重指数、血压、空腹血糖、甘油三醋、总胆固醇、谷丙转氨酶和血尿酸水平显著高于对照组(P<0.05);两组间总胆固醇和总胆红素差异无显著性(P>0.05).NAFL组空腹血胰岛素、胰岛素抵抗指数(HOMA-IR)水平明显升高(P<0.01).NAFL组合并肥胖、高血压、高甘油三酯血症和(或)低高密度脂蛋白胆固醇血症、高血糖和代谢综合征显著高于对照组(70.77%vs 20.83%、54.93% vs 29.17%、62.32%vs 21.88%、48.59% vs 15.63%、39.08% vs 8.33%).两组中119例有代谢综合征,其中有NAFL占93.28%,肥胖占88.23%,高血压占87.40%,血脂紊乱占92.44%,高血糖占65.55%.结论NAFL患者存在明显的代谢综合征各组分集聚的特征,代谢综合征患病率明显升高.因此NAFL是代谢综合征的一个危险因素. 相似文献
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代谢综合征的流行病学研究进展 总被引:1,自引:0,他引:1
代谢综合征(metabolic syndrome,MS)是一组以肥胖、高血压、糖代谢及血脂异常等为主要临床表现的症候群。1988年Reaven[1]首次提出了"X综合征"这一概念,1999年WHO和2001年美国国家胆固醇教育委员会成年治疗组(NCEP-ATPⅢ)统一将其命名为代谢综合征,即糖调节减损或糖尿病,和/或胰岛素抵抗,并伴有另外二项或三项以上的成份,如高血压、高甘油三酯血症和/或低HDL-C血症、中心性肥胖或微量蛋白尿。 相似文献
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糖尿病是代谢综合征(MS)或胰岛素抵抗综合征(IR)的重要组成部分,80%以上的2型糖尿病合并MS。代谢综合征(MS),又称胰岛素抵抗综合征(IR),最早提出于1779年,Fronzo等应用正常血糖高胰岛素钳夹技术(Euglyeenic Hyperinsulinemic Clamp Technique)测定患者的胰岛素敏感性,结果发现:肥胖、2型糖尿病、高血压、高甘油三酯血症/低高密度脂蛋白血症和动脉粥样硬化等疾病患者多存在胰岛素抵抗和高胰岛素血症。随后各国学者在此领域进行了深入而广泛的研究。 相似文献
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Overweight, obesity and the metabolic syndrome occur in genetically susceptible individuals with environmental influences, and may be further compounded by other disorders of metabolism or pharmacological therapy that increase insulin resistance or promotes weight gain. Treatment of the metabolic syndrome should focus on treatment on [corrected] each individual component, but first, lifestyle modification, including diet and exercise with weight reduction, should be [corrected] the foundation of any successful treatment regimen for the metabolic syndrome. Pharmacological therapy should be individualized and targeted to normalize blood pressure, HDL cholesterol, triglycerides and glucose values. If successful, comprehensive management of the metabolic syndrome promises to delay or prevent the development of coronary heart disease and Type 2 diabetes mellitus. 相似文献
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《Expert opinion on pharmacotherapy》2013,14(13):2059-2075
Overweight, obesity and the metabolic syndrome occur in genetically susceptible individuals with environmental influences, and may be further compounded by other disorders of metabolism or pharmacological therapy that increase insulin resistance or promotes weight gain. Treatment of the metabolic syndrome should focus on each individual component, but first, lifestyle modification, including diet and exercise with weight reduction, should be the foundation of any successful treatment regimen for the metabolic syndrome. Pharmacological therapy should be individualized and targeted to normalize blood pressure, HDL cholesterol, triglycerides and glucose values. If successful, comprehensive management of the metabolic syndrome promises to delay or prevent the development of coronary heart disease and Type 2 diabetes mellitus. 相似文献
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Smith SR 《Current drug targets. CNS and neurological disorders》2004,3(5):431-439
The metabolic syndrome is a cluster of easy-to-measure clinical phenotypes that serve as markers for increased risk for CVD and diabetes. There is no universal agreement as to the underlying pathophysiology of the metabolic syndrome. At its core, the metabolic syndrome is the result of energy excess; therefore treating obesity is a good strategy to reverse the clinical features of the metabolic syndrome. Hypertension is a special case, may not be part of the core pathophysiology of the metabolic syndrome, and will not be discussed. After a brief review of recent developments in the pathophysiology of the metabolic syndrome, this review will concentrate on peripheral targets in the following categories: ectopic fat and fat oxidation, intrinsic defects in substrate switching and mitochondrial biogenesis, lipolysis and lipid turnover, adipose tissue as an endocrine organ, nutrient / energy sensing systems, and inflammation. The advantages and pitfalls of these targets will be discussed with an eye towards the relevant literature. 相似文献
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Sinagra D Amato C Scarpilta AM Brigandì M Amato M Saura G Latteri MA Caimi G 《European review for medical and pharmacological sciences》2002,6(2-3):55-59
States of hyperinsulinemia with insulin resistance are frequently associated with proliferative tissue abnormalities, via stimulation of DNA synthesis and cell proliferation through the IGF-1 receptor. Such elements of metabolic syndrome (hyperinsulinemia/insulin-resistance, obesity, type 2 diabetes mellitus, hypertension, dyslipidemia) are explored in a population of 125 women (n. 50 with histologically confirmed diagnosis of breast cancer, Group A; n. 50 with benign breast pathology, Group B; n. 25 with no breast pathology, Group C, controls), affering to a Center for the prevention of breast cancer, in order to investigate for an eventual relationship between these pathologies. The prevalence of type 2 diabetes mellitus, hypertension, dyslipidemia, was higher in group of women affected by breast cancer vs. benign breast pathology and controls. This finding is in agreement with the hypothesis of the interrelationship of hyperinsulinism/insulin resistance with the growth-related abnormalities of breast cancer. 相似文献
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While on holiday in Zimbabwe, a forty-one year old woman with a long history of intermittent psychiatric illness developed what was diagnosed as neuroleptic malignant syndrome. She was admitted to the Intensive Care Unit of Harare Central Hospital and was treated successfully with bromocriptine and dantrolene. 相似文献
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Schill D 《Medizinische Monatsschrift für Pharmazeuten》2005,28(10):370-371