Nuclear magnetic resonance reveals postprandial low-density lipoprotein cholesterol determined by enzymatic method could be a misleading indicator.

BACKGROUND

Serum concentration of low-density lipoprotein cholesterol (LDL-C) is markedly reduced after a meal. Does postprandial cholesterol in LDL truly decline via clearance of LDL particles or is there simply a redistribution of cholesterol in LDL subclasses? Thus, we sought to evaluate whether postprandial decline of LDL-C reflects a reduction of LDL particle and to assess the correlation between proprotein convertase subtilisin/kexin type 9 (PCSK9) concentration and postprandial atherogenic lipoproteins profile.

METHODS

Eighty-seven persons were enrolled in this study. We measured lipid profiles by enzymatic and nuclear magnetic resonance (NMR)-based methods and serum PCSK9 concentration by enzyme-linked immunosorbent assays before and after a meal. Plasma samples were collected after a 10-h fasting and 2 and 4 h post-meal.

RESULTS

Compared to the fasting status, there was significant postprandial decline of LDL-C measured enzymatically (LDL-Ce) at 2nd and 4th h [99.38 (80.43, 120.65) vs 95.51 (74.25, 117.17) vs 87.01 (69.99, 108.28) mg/dl, p < 0.000]. But there was no significant reduction in LDL particle and its cholesterol content (LDL-Cn) determined by NMR. Just the postprandial large LDL particle [186.45 (151.36, 229.42) vs 176.92 (147.43, 220.91) vs 181.77 (149.05, 224.17), p < 0.000] and its cholesterol content [19.10 (15.09, 22.37) vs 18.28 (14.59, 21.84) vs 17.79 (14.62, 22.14), p < 0.000] were greatly decreased at 2nd and 4th h compared to the fasting one. Interestingly, postprandial serum PCSK9 was decreased at 2nd and 4th h compared with fasting concentration [298.75 (233.25, 396.92) vs 257.34 (207.52, 342.36) vs 250.57 (215.02, 339.66) ng/ml, p < 0.000]. The postprandial percent decrease in serum PCSK9 at 4th h was positively correlated to the percent decline in postprandial LDL-Ce (r = 0.252, p = 0.019) but was independently associated with the percent increase in remnant cholesterol (r = 0.262, p = 0.016).

CONCLUSIONS

Postprandial decline of LDL-C determined enzymatically was not confirmed by NMR-based methods. Indeed, there exists cholesterol redistribution in LDL subclasses following a meal. The decrease of postprandial PCSK9 may be secondary to the increase in intrahepatic lipids following food intake.