The influence of obesity and consequent insulin resistance on coronary risk factors in medically treated patients with coronary disease.
The influence of obesity and consequent insulin resistance on coronary risk factors in medically treated patients with coronary disease.
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肥胖和随之而来的胰岛素抵抗对接受治疗的冠心病患者的冠心病危险因素的影响。
DOI：
10.1038/ijo.2008.6
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发表时间：
2008
期刊：
影响因子：
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通讯作者：
Ludlow,M
中科院分区：
文献类型：
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作者：
Ades,PA;Savage,PD;Toth,MJ;Schneider,DJ;Audelin,MC;Bunn,JY;Ludlow,M
目的：肥胖在一定程度上通过与高脂血症、高血压、凝血异常和胰岛素抵抗的相关性来促进冠心病（CHD）的发生和进展。我们评估了这些关系在接受循证预防性药物治疗的已确诊 CHD 患者中是否持续存在。 设计和受试者：我们对 74 名患有 CHD 且体重指数 (BMI) > 27 kg m–2（平均 32±4）的成人进行了一项横断面研究。受试者的平均年龄为 64±9 岁（范围 44-84 岁）。测量：肥胖测量包括体重、BMI、腰围、脂肪量、腹内脂肪和皮下脂肪。危险因素测量包括胰岛素敏感性、空腹胰岛素水平、血脂、血压、C反应蛋白（hs-CRP）、纤溶酶原激活剂抑制剂（PAI-1）和血小板反应性。药物使用包括阿司匹林 (99%)、他汀类药物 (84%)、β 受体阻滞剂 (71%)、ACE 抑制剂或阻滞剂 (37%) 和氯吡格雷 (28%)。 结果：除了内脏脂肪和 hs-CRP 之间存在适度关系外，肥胖参数与脂质浓度、血压、凝血异常或血小板反应性等危险因素测量值之间没有直接关系（r= 0.30，P= 0.02）。然而，BMI、腰围、脂肪量、腹部总脂肪和腹部皮下脂肪的增加均与胰岛素敏感性（r值−0.30至−0.45，P值0.01至<0.001）和胰岛素浓度相关。反过来，胰岛素敏感性是 PAI-1、甘油三酯、高密度脂蛋白 (HDL) 水平、胆固醇/HDL 水平（所有 P< 0.01）和血小板反应性（R= 0.34，P= 0.02）的最佳预测因子。结论：预防性药物治疗的使用消除了肥胖与 CHD 危险因素之间的预期关系。然而，胰岛素抵抗的残余影响却没有得到治疗。总肥胖和中心性肥胖是胰岛素敏感性的强预测因子，而胰岛素敏感性又可预测心脏危险因素，如脂质浓度、PAI-1 和血小板反应性。因此，虽然循证药物治疗可能会削弱肥胖与许多心脏危险因素之间的统计关系，但肥胖会降低组织胰岛素敏感性，从而对冠心病风险产生负面影响。
Objective:Obesity promotes the development and progression of coronary heart disease (CHD), in part, through its association with hyperlipidemia, hypertension, clotting abnormalities and insulin resistance. We assessed whether these relationships persist in patients with established CHD treated with evidence-based preventive pharmacologic therapies.Design and subjects:We performed a cross-sectional study of 74 adults with CHD and a body mass index (BMI) of> 27 kg m–2 (mean 32±4). The mean age of subjects was 64±9 years (range 44–84 years).Measurements:Obesity measures included weight, BMI, waist, fat mass, intra-abdominal fat and subcutaneous fat. Risk factor measures included insulin sensitivity, fasting insulin level, lipid profiles, blood pressure, C-reactive protein (hs-CRP), plasminogen activator inhibitor (PAI-1) and platelet reactivity. Medication use included aspirin (99%), statin (84%), β-blocker (71%), ACE inhibitor or blocker (37%) and clopidogrel (28%).Results:There was no direct relationship between obesity parameters and risk factor measures of lipid concentrations, blood pressure, clotting abnormalities or platelet reactivity except for a modest relationship between visceral fat and hs-CRP (r= 0.30, P= 0.02). However, increased BMI, waist circumference, fat mass, total abdominal fat and abdominal subcutaneous fat all correlated with insulin sensitivity (r-values− 0.30 to− 0.45, P-values 0.01 to< 0.001) and insulin concentrations. Insulin sensitivity, in turn, was the best predictor of PAI-1, triglycerides, high-density lipoprotein (HDL) levels, cholesterol/HDL levels (all P< 0.01) and platelet reactivity (R= 0.34, P= 0.02).Conclusions:Use of preventive pharmacologic therapies obviated the expected relationship between adiposity and CHD risk factors. However, a residual effect of insulin resistance is left untreated. Total adiposity and central adiposity were strong predictors of insulin sensitivity, which in turn predicted cardiac risk factors such as lipid concentrations, PAI-1 and platelet reactivity. Thus, while evidence-based pharmacologic treatments may diminish the statistical relationship between obesity and many cardiac risk factors, adiposity negatively impacts CHD risk by reducing tissue insulin sensitivity.