ReviewNutrients2019
Supplementary Nitric Oxide Donors and Exercise as Potential Means to Improve Vascular Health in People with Type 1 Diabetes: Yes to NO?
Review in Nutrients, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- Acute effects of combined supplementation of L-arginine and citrulline malate on aerobic, anaerobic, and CrossFit exercise performance.Scientific reports · 2025Trial
- S-Nitrosylation in Cardiovascular Disorders: The State of the Art.Biomolecules · 2025Review
- L-Arginine and Nitric Oxide in Vascular Regulation-Experimental Findings in the Context of Blood Donation.Nutrients · 2025Review
- Astragaloside IV prevents endothelial dysfunction by improving oxidative stress in streptozotocin-induced diabetic mouse aortas.Experimental and therapeutic medicine · 2021Article
- Type 1 diabetes patients increase CXCR4Scientific reports · 2021Article
- Circulating biomarkers of nitric oxide bioactivity and impaired muscle vasoreactivity to exercise in adults with uncomplicated type 1 diabetes.Diabetologia · 2021 · on this mapArticle
- Roles of Nitric Oxide in the Regulation of Reproduction: A Review.Frontiers in endocrinology · 2021Review
- Endothelial Hyper-Permeability Induced by T1D Sera Can be Reversed by iNOS Inactivation.International journal of molecular sciences · 2020Article
- Activated whole-body arginine pathway in high-active mice.PloS one · 2020Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.