Postprandial endothelial function does not differ in women by race: an insulin resistance paradox?

Postprandial endothelial function does not differ in women by race: an insulin resistance paradox?
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不同种族女性的餐后内皮功能没有差异:胰岛素抵抗悖论?

DOI:
10.1152/ajpendo.00434.2011
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发表时间:
2012
期刊:
American journal of physiology. Endocrinology and metabolism
影响因子:
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通讯作者:
Sumner,AnneE
Sumner,AnneE
中科院分区:
--
文献类型:
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作者:
Muniyappa,Ranganath;Sachdev,Vandana;Sidenko,Stanislav;Ricks,Madia;Castillo,DarleenC;Courville,AmberB;Sumner,AnneE

文献摘要

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胰岛素抵抗与内皮功能障碍有关。由于非洲裔美国女性比白人女性更容易产生胰岛素抵抗,因此人们认为非洲裔美国女性的内皮功能受损。然而,餐后内皮功能的种族差异尚未得到研究。在这项研究中,我们检验了以下假设:与白人女性相比,非洲裔美国女性餐后内皮功能受损。研究人员对 36 名年龄和体重指数 (BMI) 匹配(年龄:37 ± 11 岁;BMI:30 ± 6 kg/m2)女性(18 名非裔美国女性,18 名白人女性)早餐(20% 蛋白质、40% 脂肪和 40% 碳水化合物)后的餐后内皮功能进行了评估。餐后 0、2、4 和 6 小时测量内皮功能,定义为肱动脉血流介导的扩张 (FMD) 的百分比变化。各组之间的基线FMD、全身脂肪、腹部内脏脂肪以及空腹血糖、胰岛素、总胆固醇、低密度脂蛋白胆固醇或血清雌二醇水平没有显着差异。尽管非洲裔美国女性的胰岛素敏感性较低[胰岛素敏感性指数(平均值±标准差):3.6 ± 1.5 vs. 5.2 ± 2.6,P= 0.02],但空腹甘油三酯(TG:56 ± 37 vs. 97 ± 49 mg/dl,P= 0.007)和增量TG曲线下面积(AUC0-6小时:279 ± 190) vs. 492 ± 255 mg·dl−1·min−1·10−2,P= 0.008)非裔美国人低于白人女性。早餐与白人和非洲裔美国人的 FMD 显着增加相关,但各组之间的餐后 FMD 没有显着差异(组 × 时间交互作用 P> 0.1)。尽管存在胰岛素抵抗,非裔美国女性的餐后内皮功能与白人女性相当。这些结果意味着胰岛素敏感性可能不是内皮功能种族差异的重要决定因素。
Insulin resistance is associated with endothelial dysfunction. Because African-American women are more insulin-resistant than white women, it is assumed that African-American women have impaired endothelial function. However, racial differences in postprandial endothelial function have not been examined. In this study, we test the hypothesis that African-American women have impaired postprandial endothelial function compared with white women. Postprandial endothelial function following a breakfast (20% protein, 40% fat, and 40% carbohydrate) was evaluated in 36 (18 African-American women, 18 white women) age- and body mass index (BMI)-matched (age: 37 ± 11 yr; BMI: 30 ± 6 kg/m2) women. Endothelial function, defined by percent change in brachial artery flow-mediated dilation (FMD), was measured at 0, 2, 4, and 6 h following a meal. There were no significant differences between the groups in baseline FMD, total body fat, abdominal visceral fat, and fasting levels of glucose, insulin, total cholesterol, low-density lipoprotein cholesterol, or serum estradiol. Although African-American women were less insulin-sensitive [insulin sensitivity index (mean ± SD): 3.6 ± 1.5 vs. 5.2 ± 2.6,P= 0.02], both fasting triglyceride (TG: 56 ± 37 vs. 97 ± 49 mg/dl,P= 0.007) and incremental TG area under the curve (AUC0–6hr: 279 ± 190 vs. 492 ± 255 mg·dl−1·min−1·10−2,P= 0.008) were lower in African-American than white women. Breakfast was associated with a significant increase in FMD in whites and African-Americans, and there was no significant difference in postprandial FMD between the groups (P> 0.1 for group × time interactions). Despite being insulin-resistant, postprandial endothelial function in African-American women was comparable to white women. These results imply that insulin sensitivity may not be an important determinant of racial differences in endothelial function.