Dietary sodium intake relates to vascular health in children with type 1 diabetes

2017 ◽  
Vol 19 (1) ◽  
pp. 138-142 ◽  
Author(s):  
Jemma Anderson ◽  
Jennifer J Couper ◽  
Sarah Toome ◽  
Christine Mpundu-Kaambwa ◽  
Lynne C Giles ◽  
...  
Diabetes Care ◽  
2011 ◽  
Vol 34 (4) ◽  
pp. 861-866 ◽  
Author(s):  
M. C. Thomas ◽  
J. Moran ◽  
C. Forsblom ◽  
V. Harjutsalo ◽  
L. Thorn ◽  
...  

2013 ◽  
Vol 124 (10) ◽  
pp. 617-626 ◽  
Author(s):  
Chris Tikellis ◽  
Raelene J. Pickering ◽  
Despina Tsorotes ◽  
Valma Harjutsalo ◽  
Lena Thorn ◽  
...  

It is recommended that individuals with diabetes restrict their dietary sodium intake. However, although salt intake is correlated with BP (blood pressure), it also partly determines the activation state of the RAAS (renin–angiotensin–aldosterone system), a key mediator of diabetes-associated atherosclerosis. apoE KO (apolipoprotein E knockout) mice were allocated for the induction of diabetes with streptozotocin or citrate buffer (controls) and further randomized to isocaloric diets containing 0.05%, 0.3% or 3.1% sodium with or without the ACEi [ACE (angiotensin-converting enzyme) inhibitor] perindopril. After 6 weeks of study, plaque accumulation was quantified and markers of atherogenesis were assessed using RT–PCR (reverse transcription–PCR) and ELISA. The association of sodium intake and adverse cardiovascular and mortality outcomes were explored in 2648 adults with Type 1 diabetes without prior CVD (cardiovascular disease) from the FinnDiane study. A 0.05% sodium diet was associated with increased plaque accumulation in diabetic apoE KO mice, associated with activation of the RAAS. By contrast, a diet containing 3.1% sodium suppressed atherogenesis associated with suppression of the RAAS, with an efficacy comparable with ACE inhibition. In adults with Type 1 diabetes, low sodium intake was also associated with an increased risk of all-cause mortality and new-onset cardiovascular events. However, high sodium intake was also associated with adverse outcomes, leading to a J-shaped relationship overall. Although BP lowering is an important goal for the management of diabetes, off-target actions to activate the RAAS may contribute to an observed lack of protection from cardiovascular complications in patients with Type 1 diabetes with low sodium intake.


2016 ◽  
Vol 31 (6) ◽  
pp. 1354-1362 ◽  
Author(s):  
F. Yarde ◽  
W. Spiering ◽  
A. Franx ◽  
F.L.J. Visseren ◽  
M.J.C. Eijkemans ◽  
...  

Author(s):  
Angela Zanfardino ◽  
Angela Zanfardino ◽  
Pierluigi Marzuillo ◽  
Linda Sessa ◽  
Assunta S Rollato ◽  
...  

Aim: People around the world are consuming much more sodium than is physiologically necessary. A number of studies suggest that dietary sodium intake is related to weight gain. The aim of our study was to evaluate in a population of children and adolescents with type 1 diabetes mellitus, possible correlations between the urinary sodium excretion (UNa24h), indirect marker of sodium intake, and both duration of diabetes and BMI z-score. Moreover, we also evaluated the correlation between UNa24h and duration of diabetes according with the presence/absence of overweight/obesity. Research Design and Methods: Children and adolescents aged between 4 and 18 years with type 1 diabetes were consecutively enrolled from Regional Center for Pediatric Diabetes in Naples. Urinary sodium concentrations were tested in three 24 h urine samples of 68 individuals (204 tests). Results: Mean UNa24h was 141.3±68.2 mmol/24h corresponding to 8.1±3.9 gr of NaCl intake. Seventyfive percent of subjects aged between 4 and 6 years, 95% of subjects aged between 7 and 10 years and 79.5% of subjects aged between 11 and 18 years consume more salt of the LARN’s advice. Urinary sodium excretion increased in relation to the increase of duration, in years, of diabetes (p=0.0027). No statistically significant relationship is between UNa24h (mmol/24h) and zBMI (p=0.705). Conclusions: This study shows that young patients with type 1 diabetes have high levels of UNa24h. Given the close correlation between the UNa24h and salt intake we can conclude that they take more salt with their diet. High salt intake is not related to overweight but to diabetes duration.


2000 ◽  
Vol 278 (5) ◽  
pp. E917-E924 ◽  
Author(s):  
Michael W. Brands ◽  
Sharyn M. Fitzgerald ◽  
William H. Hewitt ◽  
Allison E. Hailman

Recently we reported that hindquarter blood flow, measured 24 h/day, decreased progressively over the first 6 days of type 1 diabetes in rats. That response, coupled with the tendency of mean arterial pressure to increase, suggested a vasoconstrictor response. The purpose of this study was to measure the changes in cardiac output together with the renal hemodynamic and excretory responses to allow integrative determination of whether vasoconstriction likely accompanies the onset of type 1 diabetes. Rats were instrumented with a Transonic flow probe on the ascending aorta and with artery and vein catheters, and cardiac output and mean arterial pressure were measured continuously, 24 h/day, throughout the study. The induction of diabetes, by withdrawing intravenous insulin-replacement therapy in streptozotocin-treated rats, caused a progressive decrease in cardiac output that was 85 ± 5% of control levels by day 7. This was associated with significant increases in glomerular filtration rate, renal blood flow, and microalbuminuria as well as urinary fluid and sodium losses, with a negative cumulative sodium balance averaging 15.7 ± 1.6 meq by day 7. Restoring insulin-replacement therapy reversed the renal excretory responses but did not correct the negative sodium balance, yet cardiac output returned rapidly to control values. Increasing sodium intake during the diabetic and recovery periods also did not significantly affect the cardiac output response during any period. These results indicate that cardiac output decreases significantly at the onset of type 1 diabetes without glycemic control, and although volume loss may contribute to this response, there also is a component that is not volume or sodium dependent. We suggest this may be due to vasoconstriction, but to what extent local blood flow autoregulation or active vasoconstriction may have mediated that response is not known.


Circulation ◽  
2018 ◽  
Vol 138 (25) ◽  
pp. 2895-2907 ◽  
Author(s):  
Petter Bjornstad ◽  
Michal Schäfer ◽  
Uyen Truong ◽  
Melanie Cree-Green ◽  
Laura Pyle ◽  
...  

2016 ◽  
Vol 30 (6) ◽  
pp. 1144-1150 ◽  
Author(s):  
Aila J. Ahola ◽  
Riitta Freese ◽  
Sari Mäkimattila ◽  
Carol Forsblom ◽  
Per-Henrik Groop

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Alice Tamara ◽  
David J. Coulson ◽  
Jevi Septyani Latief ◽  
Sherin Bakhashab ◽  
Jolanta U. Weaver

Abstract Background In spite of clinical progress, cardiovascular disease (CVD) remains the predominant cause of mortality worldwide. Overexpression studies in animals have proven miR-424-5p to have anti-angiogenic properties. As type 1 diabetes mellitus (T1DM) without CVD displays endothelial dysfunction and reduced circulating endothelial progenitor cells (cEPCs), it offers a model of subclinical CVD. Therefore, we explored miR-424-5p, cytokines and vascular health in T1DM. Methods Twenty-nine well-controlled T1DM patients with no CVD and 20-matched controls were studied. Cytokines IL8, TNF-α, IL7, VEGF-C, cEPCs/CD45dimCD34+CD133+ cells and ex-vivo proangiogenic cells (PACs)/fibronectin adhesion assay (FAA) were measured. MiR-424-5p in plasma and peripheral blood mononuclear cells (PBMC) along with mRNAs in PBMC was evaluated. Results We found an elevation of IL7 (p = 0.008), IL8 (p = 0.003), TNF-α (p = 0.041), VEGF-C (p = 0.013), upregulation of mRNA CXCR1 (p = 0.009), CXCR2 (p < 0.001) and reduction of cEPCs (p < 0.001), PACs (p < 0.001) and FAA (p = 0.017) in T1DM. MiR-424-5p was upregulated in T1DM in PBMC (p < 0.001). MiR-424-5p was negatively correlated with cEPCs (p = 0.006), PACs (p = 0.005) and FAA (p < 0.001) and positively with HbA1c (p < 0.001), IL7 (p = 0.008), IL8 (p = 0.017), VEGF-C (p = 0.007), CXCR1 (p = 0.02) and CXCR2 (p = 0.001). ROC curve analyses showed (1) miR-424-5p to be a biomarker for T1DM (p < 0.001) and (2) significant upregulation of miR-424-5p, defining subclinical CVD, occurred at HbA1c of 46.5 mmol/mol (p = 0.002). Conclusion We validated animal research on anti-angiogenic properties of miR-424-5p in T1DM. MiR-424-5p may be a biomarker for onset of subclinical CVD at HbA1c of 46.5 mmol/mol (pre-diabetes). Thus, miR-424-5p has potential use for CVD monitoring whilst anti-miR-424-5p-based therapies may be used to reduce CVD morbidity/mortality in T1DM.


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