Key result
Oral fat loading induced a shift toward smaller LDL phenotypes in 3 of 8 patients with pattern A and 7 of 35 patients with pattern I, driven by higher postprandial triglyceride-rich lipoproteins.
Why the study?
Does an oral fat load alter LDL particle size and phenotype in patients with myocardial infarction?
Observational (n=63)
Does an oral fat load alter LDL particle size and phenotype in patients with myocardial infarction?
Alimentary lipemia plays an important role in remodeling LDL particles into more atherogenic small, dense LDLs in patients with a history of myocardial infarction.
Answers are grounded in this paper and cite their sources.
Postprandial lipemia may promote atherogenic LDL shifts post-MI; leaves open whether dietary fat restriction improves outcomes.
BACKGROUND: Low-density lipoprotein (LDL) particle size is strongly affected by both fasting and postprandial triglyceride levels. We report here that the LDL phenotype shifts toward the smaller phenotype during oral fat tolerance tests (OFTTs) in some patients with myocardial infarction (MI); a condition closely associated with postprandial increases of triglyceride and remnant-like particles (RLPs). METHODS: Oral fat tolerance tests were performed on 63 MI patients with fasting serum triglyceride levels of less than 2.25 mmol L-1 (= 200 mg dL-1). Remnant-like particles and other serum lipids were compared among patients characterized by three LDL phenotypes based on nondenaturing gradient gel electrophoresis: pattern A (large LDLs, peak LDL particle size > or = 260 A), pattern I (intermediate-sized LDLs, LDL size > 255 A, < 260 A), and pattern B (small, dense LDLs, LDL size < or = 255 A). RESULTS: The LDL size decreased significantly in patients with the highest tertile of areas under the incremental curves (AUICs) of triglycerides above the fasting levels. The LDL phenotype shifted toward the smaller phenotype after a fat load in three of eight patients with pattern A and in seven of 35 patients with pattern I. The AUICs of triglyceride-rich lipoproteins were significantly higher in these patients than in the patients exhibiting little change in LDL size, whereas the fasting metabolic parameters were similar among the patients of the same LDL phenotype in the fasting state. CONCLUSION: These results suggest that alimentary lipaemia plays an important role in the remodeling of LDL particles into the more atherogenic small, dense LDLs in patients with MI.
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Koba et al. (2005) conducted an observational in myocardial infarction (n=63). Oral fat tolerance test was evaluated on Change in LDL particle size and phenotype. Oral fat loading induced a shift toward smaller LDL phenotypes in 3 of 8 patients with pattern A and 7 of 35 patients with pattern I, driven by higher postprandial triglyceride-rich lipoproteins.
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