Pierce Gary L, Beske Stacy D, Lawson Brooke R, Southall Kara L, Benay Francoise J, Donato Anthony J, Seals Douglas R
Department of Integrative Physiology, UCB 354, University of Colorado, Boulder, CO 80309, USA.
Hypertension. 2008 Jul;52(1):72-9. doi: 10.1161/HYPERTENSIONAHA.108.111427. Epub 2008 May 26.
Obesity is associated with vascular endothelial dysfunction, as indicated by impaired endothelium-dependent dilation. Presently there is no direct evidence that energy intake-restricted weight loss alone improves conduit or resistance artery endothelium-dependent dilation, the mechanisms involved, or whether improvements differ with patient age. A total of 40 overweight or obese (body mass index: >or=25<40 kg/m(2)) nondiabetic men and women aged 21 to 69 years completed 12 weeks of reduced energy intake (n=26; 15 male) or attention control (n=14; 9 male) and 4 weeks of weight maintenance (randomized trial). Energy intake restriction reduced estimated total energy intake (33%), body weight (10.5%), total and abdominal body fat, plasma leptin, oxidized low-density lipoprotein, and improved several metabolic risk factors. Brachial artery flow-mediated dilation was increased by 30% (6.0+/-0.7% versus 7.9+/-0.7%Delta; P=0.01; n=17). Peak forearm blood flow during intrabrachial artery infusion of acetylcholine was increased by 26% (16.8+/-1.4 versus 21.1+/-1.9 mL/100 mL per minute; P<0.05; n=15); this was inversely related to the reduction in the abdominal visceral:subcutaneous fat ratio (r=-0.46; P<0.05) and was abolished by inhibition of NO synthesis with N(G)-monomethyl-L-arginine. Improvements in endothelium-dependent dilation were not related to age: mean increases in subjects >50 years of age were similar to or greater than those <50 years of age. Energy intake-restricted weight loss alone is an effective intervention for improving peripheral conduit and resistance artery endothelial function in young and older overweight/obese adults. The improvements in resistance artery function are mediated by an increase in NO bioavailability and are related to reductions in abdominal visceral fat.
肥胖与血管内皮功能功能功能功能障碍相关，这可通过内皮依赖性舒张功能受损得以体现。目前尚无直接证据表明单纯限制能量摄入的体重减轻能够改善传导动脉或阻力动脉的内皮依赖性舒张功能、其中涉及的机制，以及改善情况是否因患者年龄而异。共有40名年龄在21至69岁之间的超重或肥胖（体重指数：≥25＜40kg/m²）非糖尿病男性和女性完成了12周的能量摄入减少（n = 26；15名男性）或注意力控制（n = 14；9名男性）以及4周的体重维持期（随机试验）。能量摄入限制降低了估计的总能量摄入（33%）、体重（10.5%）、全身及腹部体脂、血浆瘦素、氧化型低密度脂蛋白，并改善了多种代谢危险因素。肱动脉血流介导的舒张功能增加了30%（6.0±0.7%对7.9±0.7%Δ；P = 0.01；n = 17）。肱动脉内注入乙酰胆碱期间前臂血流峰值增加了26%（16.8±1.4对21.1±1.9mL/100mL每分钟；P＜0.05；n = 15）；这与腹部内脏脂肪与皮下脂肪比值的降低呈负相关（r = -0.46；P＜0.05），并且被N(G)-单甲基-L-精氨酸抑制一氧化氮合成所消除。内皮依赖性舒张功能的改善与年龄无关：50岁以上受试者的平均增加幅度与50岁以下受试者相似或更大。单纯限制能量摄入的体重减轻是改善年轻及年长超重/肥胖成年人外周传导动脉和阻力动脉内皮功能的有效干预措施。阻力动脉功能的改善是由一氧化氮生物利用度增加介导的，并且与腹部内脏脂肪的减少有关。
