Sodium Intake, Circulating Microvesicles and Cardiovascular Outcomes in Type 2 Diabetes

Abstract

There is ongoing debate surrounding the complex relationship between dietary sodium intake and cardiovascular morbidity and mortality. The existing literature consists largely of observational studies that have demonstrated positive, negative, U-/J-shaped or unclear associations between sodium intake and cardiovascular outcomes. Our group and others have previously demonstrated an inverse relationship between dietary sodium intake and cardiovascular outcomes in people with type 2 diabetes. Increased activity of the renin-angiotensin-aldosterone system and sympathetic nervous system is postulated to contribute to these paradoxical findings through endothelial dysfunction, a precursor to the development of cardiovascular disease. Microvesicles are submicron (0.1 – 1.0μm) vesicles that form during cellular activation, injury or death with endothelial microvesicles being recognized markers of endothelial dysfunction. They are pathologically elevated in a variety of vascular-related conditions including type 2 diabetes. Lower habitual sodium intake in type 2 diabetes has been associated with higher pro-coagulant platelet microvesicles levels but not with endothelial microvesicles. Research utilizing endothelial microvesicles to evaluate the mechanistic relationship between dietary sodium intake and adverse cardiovascular outcomes in type 2 diabetes remains scarce.

Association between glutathione peroxidase‐3 activity and carotid atherosclerosis in patients with type 2 diabetes mellitus

“…According to the nationally representative cross‐sectional survey in 2013 in mainland China, the prevalence of diabetes was up to 10.9% (Wang et al., 2017). People with type 2 diabetes mellitus (T2DM) have a higher risk of cardiovascular complications, such as myocardial infarction, ischemic stroke, and carotid atherosclerosis (Henning, 2018; Liu, Baqar, Lincz, & Ekinci, 2019). Ultrasound measurement of carotid intima–media thickness (CIMT) is widely recognized as a non‐invasive and reliable surrogate marker for carotid atherosclerosis (Chen et al., 2016; Everson‐Rose et al., 2014; Nambi et al., 2012; Nezu, Hosomi, Aoki, & Matsumoto, 2016; Plichart et al., 2011).…”