Dietary salt restriction increases plasma lipoprotein and inflammatory marker concentrations in hypertensive patients
Received 12 November 2007; accepted 20 December 2007. published online 13 February 2008.
Abstract
Background
Dietary salt restriction has been reported to adversely modify the plasma lipoprotein profile in hypertensive and in normotensive subjects. We investigated the effects of the low sodium intake (LSI) on the plasma lipoprotein profile and on inflammation and thrombosis biomarkers during the fasting and postprandial periods.
Methods
Non-obese, non-treated hypertensive adults (n=41) were fed strictly controlled diets. An initial week on a control diet (CD, Na=160mmol/day) was followed by 3 weeks on LSI (Na=60mmol/day). At admission and on the last day of each period, the 24-h ambulatory blood pressure was monitored and blood was drawn after an overnight fasting period and after a fat-rich test meal.
Results
The dietary adherence was confirmed by 24-h urinary sodium excretion. Fasting triglyceride (TG), chylomicron-cholesterol, hsC-reactive protein (CRP), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) concentrations, renin activity, aldosterone, insulin, and homeostasis model assessment insulin resistance (HOMA-IR) values were higher, but non-esterified fatty acids (NEFA) were lower on LSI than on CD. For LSI, areas under the curve (AUC) of TG, chylomicron-cholesterol, apoB and the cholesterol/apoB ratio were increased, whereas AUC-NEFA was lowered. LSI did not modify body weight, hematocrit, fasting plasma cholesterol, glucose, adiponectin, leptin, fibrinogen and factor VII (FVII), and AUC of lipoprotein lipase and of lipoprotein remnants.
Conclusion
LSI induced alterations in the plasma lipoproteins and in inflammatory markers that are common features of the metabolic syndrome.
aLipids Lab (LIM10), Endocrinology and Metabolism Division of Hospital das Clínicas, Faculty of Medical Sciences of the University of Sao Paulo, Sao Paulo, Brazil
bHypertension Unit, Nephrology Division of Hospital das Clinicas, Faculty of Medical Sciences of the University of Sao Paulo, Sao Paulo, Brazil
cJapan Immunoresearch Laboratories Co., Ltd., Takasaki, Gumma, Japan
dPro-Sangue Foundation, Hemocentro-SP, Sao Paulo, Brazil
Corresponding author at: Laboratório de Lípides, Faculdade de Medicina USP. Av. Dr. Arnaldo 455, s/3305, 01246-000 São Paulo, SP, Brazil. Tel.: +55 11 3062 1255; fax: +55 11 3062 1255.
1 Both the authors contributed equally to this work.
ABSTRACT