Please use this identifier to cite or link to this item: https://hdl.handle.net/2440/99550
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Type: Journal article
Title: Association of dietary sodium intake with atherogenesis in experimental diabetes and with cardiovascular disease in patients with Type 1 diabetes
Author: Tikellis, C.
Pickering, R.
Tsorotes, D.
Harjutsalo, V.
Thorn, L.
Ahola, A.
Waden, J.
Tolonen, N.
Saraheimo, M.
Gordin, D.
Forsblom, C.
Groop, P.
Cooper, M.
Moran, J.
Thomas, M.
Citation: Clinical Science, 2013; 124(10):617-626
Publisher: Portland Press
Issue Date: 2013
ISSN: 0143-5221
1470-8736
Statement of
Responsibility: 
Chris Tikellis, Raelene J. Pickering, Despina Tsorotes, Valma Harjutsalo, Lena Thorn, Aila Ahola, Johan Wadén, Nina Tolonen, Markku Saraheimo, Daniel Gordin, Carol Forsblom, Per-Henrik Groop, Mark E. Cooper, John Moran, Merlin C. Thomas
Abstract: 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.
Keywords: Dietary sodium; type 1 diabetes
Rights: © The Authors Journal compilation © 2013 Biochemical Society
DOI: 10.1042/CS20120352
Grant ID: http://purl.org/au-research/grants/nhmrc/586675
Published version: http://dx.doi.org/10.1042/cs20120352
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