Division of Geriatric Medicine, School of Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.
Division of Cardiology, School of Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.
J Clin Endocrinol Metab. 2022 Jan 18;107(2):e500-e514. doi: 10.1210/clinem/dgab715.
Vascular aging, including endothelial dysfunction secondary to oxidative stress and inflammation, increases the risk for age-associated cardiovascular disease (CVD). Low testosterone in middle-aged/older men is associated with increased CVD risk.
We hypothesized that low testosterone contributes to age-associated endothelial dysfunction, related in part to greater oxidative stress and inflammation.
This cross-sectional study included 58 healthy, nonsmoking men categorized as young (N = 20; age 29 ± 4 years; testosterone 500 ± 58 ng/dL), middle-aged/older with higher testosterone (N = 20; age 60 ± 6 years; testosterone 512 ± 115 ng/dL), and middle-aged/older lower testosterone (N = 18; age 59 ± 8 years; testosterone 269 ± 48 ng/dL). Brachial artery flow-mediated dilation (FMDBA) was measured during acute infusion of saline (control) and vitamin C (antioxidant). Markers of oxidative stress (total antioxidant status and oxidized low-density lipoprotein cholesterol), inflammation (interleukin [IL]-6 and C-reactive protein [CRP]), and androgen deficiency symptoms were also examined.
During saline, FMDBA was reduced in middle-aged/older compared with young, regardless of testosterone status (P < 0.001). FMDBA was reduced in middle-aged/older lower testosterone (3.7% ± 2.0%) compared with middle-aged/older higher testosterone (5.7% ± 2.2%; P = 0.021), independent of symptoms. Vitamin C increased FMDBA (to 5.3% ± 1.6%; P = 0.022) in middle-aged/older lower testosterone but had no effect in young (P = 0.992) or middle-aged/older higher testosterone (P = 0.250). FMDBA correlated with serum testosterone (r = 0.45; P < 0.001), IL-6 (r = -0.41; P = 0.002), and CRP (r = -0.28; P = 0.041).
Healthy middle-aged/older men with low testosterone appear to have greater age-associated endothelial dysfunction, related in part to greater oxidative stress and inflammation. These data suggest that low testosterone concentrations may contribute to accelerated vascular aging in men.
血管老化，包括氧化应激和炎症引起的内皮功能障碍，增加了与年龄相关的心血管疾病（CVD）的风险。中年/老年男性的低睾酮与 CVD 风险增加有关。
我们假设低睾酮导致与年龄相关的内皮功能障碍，部分原因是氧化应激和炎症增加。
这项横断面研究纳入了 58 名健康、不吸烟的男性，分为年轻组（N=20；年龄 29±4 岁；睾酮 500±58ng/dL）、中年/老年高睾酮组（N=20；年龄 60±6 岁；睾酮 512±115ng/dL）和中年/老年低睾酮组（N=18；年龄 59±8 岁；睾酮 269±48ng/dL）。在急性盐水（对照）和维生素 C（抗氧化剂）输注期间测量肱动脉血流介导的扩张（FMDBA）。还检测了氧化应激标志物（总抗氧化状态和氧化型低密度脂蛋白胆固醇）、炎症标志物（白细胞介素[IL]-6 和 C 反应蛋白[CRP]）和雄激素缺乏症状。
在盐水输注期间，与年轻组相比，中年/老年组的 FMDBA 降低，无论睾酮状态如何（P<0.001）。与中年/老年高睾酮组（5.7%±2.2%）相比，中年/老年低睾酮组（3.7%±2.0%）的 FMDBA 降低（P=0.021），且与症状无关。维生素 C 增加了中年/老年低睾酮组的 FMDBA（增加至 5.3%±1.6%；P=0.022），但对年轻组（P=0.992）或中年/老年高睾酮组（P=0.250）没有影响。FMDBA 与血清睾酮（r=0.45；P<0.001）、IL-6（r=-0.41；P=0.002）和 CRP（r=-0.28；P=0.041）呈正相关。
健康的中年/老年男性低睾酮似乎与年龄相关的内皮功能障碍更大有关，部分原因是氧化应激和炎症更大。这些数据表明，低睾酮浓度可能导致男性血管老化加速。
