Diagnosis and management of the metabolic syndrome - An American Heart Association/National Heart, Lung, and Blood Institute scientific statement - Executive summary
Diagnosis and management of the metabolic syndrome - An American Heart Association/National Heart, Lung, and Blood Institute scientific statement - Executive summary
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DOI：
10.1161/circulationaha.105.169405
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发表时间：
2005-10-25
期刊：
影响因子：
37.8
通讯作者：
Costa, F
中科院分区：
文献类型：
--
作者：
Grundy, SM;Cleeman, JI;Costa, F
强烈伴有胰岛素抵抗。多余的上半身脂肪可能会积聚在腹膜内（内脏脂肪）或皮下。许多研究人员声称，与任何其他脂肪组织区室相比，过多的内脏脂肪与胰岛素抵抗的关系更为密切4, 15-21；其他研究人员发现，腹部（或躯干）皮下脂肪过多也与胰岛素抵抗有显着关系。 22-27 无论内脏脂肪和腹部皮下脂肪对胰岛素抵抗的相对影响如何，腹部（或上半身）肥胖模式与胰岛素抵抗和代谢综合征的相关性比下半身肥胖更强烈。 28 上半身肥胖的一个有趣特征是脂肪组织中非酯化脂肪酸的释放异常高12,14,28；这导致脂质在脂肪组织以外的部位积累。肌肉和肝脏中的异位脂质积累似乎容易导致胰岛素抵抗29和血脂异常。 30 许多专家认为，美国日益增加的肥胖负担是代谢综合征患病率上升的驱动力。 1-4, 31, 32 这种观点需要与胰岛素抵抗假说相协调。脂肪组织代谢异常可能是问题的症结所在。肥胖人群的脂肪组织具有胰岛素抵抗性，这会提高非酯化脂肪酸水平，加剧肌肉中的胰岛素抵抗29、33，并改变肝脏代谢31；此外，肥胖的脂肪组织表现出几种脂肪因子产生异常，这些脂肪因子可能分别影响胰岛素抵抗和/或改变 ASCVD 风险。 34 其中包括炎症细胞因子、35、36 纤溶酶原激活剂抑制剂-1、37 和其他生物活性产品38-40 的产生增加；同时，潜在的保护性脂肪因子脂联素减少。 41, 42 所有这些变化都被认为是代谢危险因素的原因。事实上，如前所述，一些人表现出代谢综合征，但全身肥胖程度适中。 43, 44 值得注意的是，许多南亚人似乎天生具有胰岛素抵抗能力，45 这种情况会因轻度腹部肥胖而加剧。 14 此外，美国人口的胰岛素抵抗程度差异很大46；那些具有更多固有胰岛素抵抗的人可能会在腹部脂肪适度过量的情况下患上代谢综合征，43, 44 但即使是很少或没有固有胰岛素抵抗的人，如果他们积累了明显的腹部肥胖，也可能会患上代谢综合征。 3, 8 这些发现支持这样的观点：身体脂肪分布，特别是过量的腹部脂肪，在该综合征的病因学中起着重要作用。最近，人们注意到这种综合征与慢性、低度炎症状态有关。 47, 48 一些研究人员推测，这种类型的炎症是该综合征的基础或加剧的原因。例如，据报道，炎症细胞因子会诱导脂肪组织和肌肉中的胰岛素抵抗。 48-51 在肥胖的情况下，脂肪组织确实会产生过量的细胞因子，而脂联素的输出却减少；这些反应似乎增强了肥胖和炎症之间的联系。 35 有趣的是，即使体内脂肪总量没有增加，胰岛素抵抗者也会表现出轻度炎症的迹象。 52最后，肥胖/胰岛素抵抗受试者代谢危险因素的临床模式存在相当大的个体和种族差异。 53, 54 每个代谢风险因素的表达可能部分属于其自身的……
strongly with insulin resistance. Excess upper body fat can accumulate either intraperitoneally (visceral fat) or subcutaneously. Many investigators claim that excess visceral fat is more strongly associated with insulin resistance than any other adipose tissue compartment4, 15–21; other workers find that excess subcutaneous abdominal (or truncal) fat also carries a significant association with insulin resistance. 22–27 Regardless of the relative contributions of visceral fat and abdominal subcutaneous fat to insulin resistance, a pattern of abdominal (or upper-body) obesity correlates more strongly with insulin resistance and the metabolic syndrome than does lower-body obesity. 28 An interesting feature of upper-body obesity is an unusually high release of nonesterified fatty acids from adipose tissue12, 14, 28; this contributes to accumulation of lipid in sites other than adipose tissue. Ectopic lipid accumulation in muscle and liver seemingly predisposes to insulin resistance29 and dyslipidemia. 30 According to many experts, the increasing burden of obesity in the United States is the driving force behind the rising prevalence of the metabolic syndrome. 1–4, 31, 32 This view needs to be harmonized with the insulin resistance hypothesis. Abnormalities in adipose tissue metabolism may be the crux of the issue. Adipose tissue in obese people is insulin resistant, which raises nonesterified fatty acid levels, worsening insulin resistance in muscle29, 33 and altering hepatic metabolism31; in addition, the adipose tissue of obesity exhibits abnormalities in the production of several adipokines that may separately affect insulin resistance and/or modify risk for ASCVD. 34 These include increased production of inflammatory cytokines, 35, 36 plasminogen activator inhibitor-1, 37 and other bioactive products38–40; at the same time the potentially protective adipokine, adiponectin, is reduced. 41, 42 All of these changes have been implicated as causes of the metabolic risk factors. Indeed, as mentioned before, some individuals exhibit the metabolic syndrome with only a moderate degree of total body obesity. 43, 44 Notable are many South Asians who appear to be inherently insulin resistant, 45 a condition that is exacerbated by mild abdominal obesity. 14 Moreover, the population of the United States varies considerably in degree of insulin resistance46; those having more inherent insulin resistance can develop the metabolic syndrome with only moderate excess in abdominal fat, 43, 44 but even people with little or no inherent insulin resistance can develop the metabolic syndrome if they accumulate marked abdominal obesity. 3, 8 These findings support the idea that body fat distribution, particularly excess abdominal fat, plays an important role in the etiology of the syndrome. Recently, this syndrome has been noted to be associated with a state of chronic, low-grade inflammation. 47, 48 Some researchers speculate that inflammation of this type underlies or exacerbates the syndrome. For example, inflammatory cytokines reportedly induce insulin resistance in both adipose tissue and muscle. 48–51 In the presence of obesity, adipose tissue indeed produces cytokines in excess, whereas output of adiponectin is diminished; these responses appear to heighten the connection between obesity and inflammation. 35 Interestingly, insulin-resistant people manifest evidence of low-grade inflammation even without an increase of total body fat. 52Finally, considerable individual and ethnic variation exists in the clinical pattern of metabolic risk factors in obese/insulin-resistant subjects. 53, 54 It is likely that the expression of each metabolic risk factor falls partially under its own …