Applied Sport, Technology, Exercise and Medicine Research Centre (A-STEM), College of Engineering, Swansea University, Swansea SA1 8EN, UK.
Diabetes Research Group, Medical School, Swansea University, Swansea SA2 8QA, UK.
Nutrients. 2019 Jul 12;11(7):1571. doi: 10.3390/nu11071571.
Type 1 diabetes (T1D) is associated with a greater occurrence of cardiovascular pathologies. Vascular dysfunction has been shown at the level of the endothelial layers and failure to maintain a continuous pool of circulating nitric oxide (NO) has been implicated in the progression of poor vascular health. Biochemically, NO can be produced via two distinct yet inter-related pathways that involve an upregulation in the enzymatic activity of nitric oxide synthase (NOS). These pathways can be split into an endogenous oxygen-dependent pathway i.e., the catabolism of the amino acid L-arginine to L-citrulline concurrently yielding NO in the process, and an exogenous oxygen-independent one i.e., the conversion of exogenous inorganic nitrate to nitrite and subsequently NO in a stepwise fashion. Although a body of research has explored the vascular responses to exercise and/or compounds known to stimulate NOS and subsequently NO production, there is little research applying these findings to individuals with T1D, for whom preventative strategies that alleviate or at least temper vascular pathologies are critical foci for long-term risk mitigation. This review addresses the proposed mechanisms responsible for vascular dysfunction, before exploring the potential mechanisms by which exercise, and two supplementary NO donors may provide vascular benefits in T1D.
1 型糖尿病（T1D）与心血管病变的发生率增加有关。已经在血管内皮层水平显示出血管功能障碍，并且循环一氧化氮（NO）的持续池的维持失败与血管健康状况恶化有关。从生化角度来看，NO 可以通过两种截然不同但相互关联的途径产生，这涉及一氧化氮合酶（NOS）的酶活性上调。这些途径可以分为内源性氧依赖性途径，即氨基酸 L-精氨酸代谢为 L-瓜氨酸，同时在此过程中产生 NO，以及外源性氧非依赖性途径，即外源性无机硝酸盐转化为亚硝酸盐，然后以逐步的方式转化为 NO。尽管大量研究探讨了运动和/或已知刺激 NOS 进而促进 NO 产生的化合物对血管的反应，但很少有研究将这些发现应用于 T1D 个体，对于 T1D 患者，减轻或至少缓解血管病变的预防策略是长期风险缓解的关键重点。本综述探讨了导致血管功能障碍的拟议机制，然后探讨了运动和两种补充性一氧化氮供体可能为 T1D 提供血管益处的潜在机制。
