Plasma Lp-PLA2 mass and apoB-lipoproteins that carry Lp-PLA2 decrease after sodium

• Published in: European journal of clinical investigation Vol. 42; no. 11; pp. 1235 - 1243
• Main Authors: Constantinides, Alexander, Kerstens, Michiel N., Dikkeschei, Bert D., van Pelt, L. Joost, Tellis, Constantinos C., Tselepis, Alexandros D., Dullaart, Robin P. F.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01-11-2012; Wiley-Blackwell
• Subjects: Biological and medical sciences; Dietary sodium challenge; Diseases of the digestive system; General aspects; lipids; lipoprotein-associated phospholipase A2; lipoproteins; Medical sciences; Metabolic diseases; Radiotherapy. Instrumental treatment. Physiotherapy. Reeducation. Rehabilitation, orthophony, crenotherapy. Diet therapy and various other treatments (general aspects); renin angiotensin aldosterone system; salt sensitivity; lipoproteins renin angiotensin aldosterone system; Nutrition; Enzyme; salt sensitivity; Lipids; Esterases; Lipoprotein; lipoprotein-associated phospholipase A; Phospholipase A; Carboxylic ester hydrolases; Feeding; Blood plasma; Renin angiotensin aldosterone system; Apolipoprotein B; Mass; Medicine; Dietary sodium challenge; Salt; Sensitivity; Diet therapy; Diet; Sodium; Hydrolases; Food
• ISSN: 0014-2972; 1365-2362
• DOI: 10.1111/j.1365-2362.2012.02719.x

Eur J Clin Invest 2012; 42 (11): 1235–1243
Background  Lipoprotein‐associated phospholipase A2 (Lp‐PLA2) is a novel cardiovascular risk marker, which is predominantly complexed to apolipoprotein (apo) B‐containing lipoproteins in human plasma. As increasing dietary sodium intake may decrease plasma apoB‐containing lipoproteins, we tested whether a sodium challenge lowers plasma Lp‐PLA2 mass, as well as the levels of apoB‐containing lipoprotein particles carrying Lp‐PLA2 (apoB‐Lp‐PLA2), employing a newly developed enzyme‐linked immunosorbent assay.
Materials and methods  In 45 women and 31 men (mean age 44 ± 14 years), plasma Lp‐PLA2 mass (turbidimetric immunoassay), the level of apoB‐Lp‐PLA2, expressed in apoB concentration and lipoproteins were measured in response to a 3‐day challenge with 9 g sodium chloride tablets daily.
Results  Urinary sodium excretion increased from 165 ± 60 to 321 ± 70 mmol/24 h (P < 0·001) after salt loading. Plasma Lp‐PLA2 mass decreased from 618 (493–719) to 588 (465–698) μg/L (P < 0·001), and apoB‐Lp‐PLA2 decreased from 0·276 (0·200–0·351) to 0·256 (0·189–0·328) g LDL protein/L (P = 0·004) in response to the sodium challenge together with decreases in plasma total cholesterol, nonhigh‐density lipoprotein (HDL) cholesterol, low‐density lipoprotein (LDL) cholesterol, apolipoprotein B and the total cholesterol/HDL cholesterol ratio (P < 0·01 for all). Changes in plasma Lp‐PLA2 mass were correlated positively with changes in total cholesterol, LDL cholesterol and non‐HDL cholesterol (r = 0·260–0·276, P < 0·05 to P < 0·02), whereas changes in apoB‐Lp‐PLA2 were correlated positively with changes in non‐HDL cholesterol and in the total cholesterol/HDL cholesterol ratio (r = 0·232–0·385, P < 0·05–0·01).
Conclusion  Both plasma Lp‐PLA2 mass levels and apoB‐Lp‐PLA2 decrease in response to a short‐term oral sodium challenge.