Abstract
BackgroundEpidemiological studies have found a U-shaped relationship between serum phosphorus and cardiovascular disease (CVD). The mechanism(s) behind such a relationship are poorly understood. Phosphorus (P) is reported to improve insulin sensitivity, which is involved in lipid metabolism, and thus we were interested in determining the impact of phosphorus ingestion on postprandial lipemia, a recognized CVD risk factor.FindingsA within–subject study design was conducted, whereby 8 healthy male subjects received a high fat meal (330Kcal; 69% energy from fat; 35 mg of phosphorus) with placebo or phosphorus (500 mg) in a random order. Postprandial blood samples (~10 ml) were collected every hour for 6 hours after meal ingestion. Changes in different parameters were analyzed using a 2-factor repeated-measure ANOVA. In the phosphorus (P) supplemented group, postprandial serum P increased (p = 0.00), while changes in insulin, non-esterified fatty acids (NEFA) and triglyceride (TG) were not significantly different than that of placebo. Concurrently, phosphorus supplementation increased postprandial concentrations of apolipoprotein B48 (ApoB48) (p < 0.05) and decreased that of apolipoprotein B100 (ApoB100) (p < 0.05).ConclusionsPhosphorus supplementation (500 mg) of the meal seems to alter the different components of postprandial lipemia. These findings highlight the potential role of phosphorus in CVD.
Highlights
Postprandial lipemia (PPL) is characterized by the accumulation of triglyceride-rich lipoproteins (TRLs) and their partially hydrolyzed products that results from the absorption of digested dietary lipids in the form of chylomicrons (CM) that contain apolipoprotein B48 (ApoB48) and/or increased hepatic production of very low density lipoproteins (VLDL) that contain apolipoprotein B100 (ApoB100) [1]
Phosphorus supplementation (500 mg) of the meal seems to alter the different components of postprandial lipemia
These findings highlight the potential role of phosphorus in cardiovascular disease (CVD)
Summary
Postprandial lipemia (PPL) is characterized by the accumulation of triglyceride-rich lipoproteins (TRLs) and their partially hydrolyzed products that results from the absorption of digested dietary lipids in the form of chylomicrons (CM) that contain ApoB48 and/or increased hepatic production of very low density lipoproteins (VLDL) that contain ApoB100 [1]. Elevated serum levels of TRLs or their components (TG, ApoB48 and ApoB100) are reported to be associated with atherosclerosis and cardiovascular disease (CVD) [2] and to be predictors of their future occurrence [3]. PPL reduction is of vital clinical importance and the elucidation of factors able to regulate it can have significant clinical. Both low and high levels of serum phosphorus (P) have been associated with increased risk of CVD [8]. Phosphorus (P) is reported to improve insulin sensitivity, which is involved in lipid metabolism, and we were interested in determining the impact of phosphorus ingestion on postprandial lipemia, a recognized CVD risk factor
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
