Maeda Seiji, Jesmin Subrina, Iemitsu Motoyuki, Otsuki Takeshi, Matsuo Tomoaki, Ohkawara Kazunori, Nakata Yoshio, Tanaka Kiyoji, Goto Katsutoshi, Miyauchi Takashi
Center for Tsukuba Advanced Research Alliance, University of Tsukuba, Tsukuba, Ibaraki 305-8577, Japan.
Exp Biol Med (Maywood). 2006 Jun;231(6):1044-7.
Obesity is associated with endothelial dysfunction that may contribute to the development of diabetes, hypertension, and atherosclerosis. Endothelin-1 (ET-1), which is produced mostly by vascular endothelial cells, has potent vasoconstrictor and proliferative activity in vascular smooth muscle cells and, therefore, has been implicated in regulation of vascular tonus and the progression of atherosclerosis, suggesting that ET-1 may be important in endothelial dysfunction. We studied whether diet-induced weight loss (i.e., lifestyle modification) affects plasma ET-1 concentration in obese individuals. We measured plasma ET-1 concentration in seven obese men (age: 48 +/- 4 years old, body mass index: 27.7 +/- 0.5 kg/m2) before and after a 3-month, diet-induced weight reduction program (i.e., lifestyle modification program). Caloric restriction reduced body weight from 78 +/- 3 to 68 +/- 2 kg (P < 0.001) and resulted in 12.1 +/- 1.2% reduction in body mass index (24.3 +/- 0.3 kg/m(2), P < 0.0001). After the weight reduction program, systolic and diastolic blood pressure significantly decreased (128 +/- 7 vs. 115 +/- 4 mm Hg, P < 0.05 and 88 +/- 4 vs. 77 +/- 2 mm Hg, P < 0.01, respectively). The plasma level of ET-1 significantly decreased after the program (5.1 +/- 0.4 vs. 4.0 +/- 0.3 pg/ml, P < 0.05). The percentage systolic blood pressure reduction and percentage plasma ET-1 concentration reduction was in a linear relationship (r = 0.86, P < 0.05). Furthermore, the relationship between percentage weight reduction and percentage plasma ET-1 concentration reduction was linear (r = 0.87, P < 0.05). We conclude that weight loss by low-calorie diet (i.e., lifestyle modification) reduces plasma ET-1 concentration in obese individuals. This reduction may contribute to the improvement of obesity-induced endothelial dysfunction.
肥胖与内皮功能障碍有关，内皮功能障碍可能会促使糖尿病、高血压和动脉粥样硬化的发展。内皮素-1（ET-1）主要由血管内皮细胞产生，在血管平滑肌细胞中具有强大的血管收缩和增殖活性，因此，它与血管张力调节和动脉粥样硬化进展有关，这表明ET-1在内皮功能障碍中可能很重要。我们研究了饮食诱导的体重减轻（即生活方式改变）是否会影响肥胖个体的血浆ET-1浓度。我们测量了7名肥胖男性（年龄：48±4岁，体重指数：27.7±0.5kg/m²）在为期3个月的饮食诱导体重减轻计划（即生活方式改变计划）前后的血浆ET-1浓度。热量限制使体重从78±3kg降至68±2kg（P<0.001），体重指数降低了12.1±1.2%（降至24.3±0.3kg/m²，P<0.0001）。体重减轻计划后，收缩压和舒张压显著降低（分别为128±7mmHg对115±4mmHg，P<0.05；88±4mmHg对77±2mmHg，P<0.01）。该计划后血浆ET-1水平显著降低（5.1±0.4pg/ml对4.0±0.3pg/ml，P<0.05）。收缩压降低百分比与血浆ET-1浓度降低百分比呈线性关系（r=0.86，P<0.05）。此外，体重减轻百分比与血浆ET-1浓度降低百分比之间的关系也是线性的（r=0.87，P<0.05）。我们得出结论，低热量饮食导致的体重减轻（即生活方式改变）可降低肥胖个体的血浆ET-1浓度。这种降低可能有助于改善肥胖诱导的内皮功能障碍。
