METHODS: We evaluated the postprandial lipid metabolism in patients with normolipemic peripheral arterial disease (PAD) after the administration of an oral fat load. Total cholesterol, low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), HDL2 and HDL3 subfractions, triglycerides (TGs), lipoprotein(a), and LDL size were determined at baseline and for 8 hours after the meal. RESULTS: In patients with PAD, TGs increased significantly at the 4th, 6th, and 8th hours postprandially; in control subjects, TGs increased at the 4th and 6th hours. HDL decreased significantly at the 4th, 6th, and 8th hours in patients with PAD and at the 6th hour in control subjects. The magnitude of postprandial lipemia, expressed as "the area under the incremental curve for TGs," was higher in patients with PAD than in control subjects (770 +/- 476 vs 391 +/- 195 mg/dL at 8 hours, P <.05). Multiple-regression analysis showed that baseline TGs were positively related to the magnitude of postprandial lipemia (P =.01) and that LDL size was negatively related (P =.05). CONCLUSIONS: This is the first documentation of postprandial behavior in patients with normolipemic PAD, suggesting the relevance of postprandial lipoprotein metabolism in the pathogenesis of peripheral atherosclerosis.
METHODS: We evaluated the postprandial lipid metabolism in patients with normolipemic peripheral arterial disease (PAD) after the administration of an oral fat load. Total cholesterol, low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), HDL2 and HDL3 subfractions, triglycerides (TGs), lipoprotein(a), and LDL size were determined at baseline and for 8 hours after the meal. RESULTS: In patients with PAD, TGs increased significantly at the 4th, 6th, and 8th hours postprandially; in control subjects, TGs increased at the 4th and 6th hours. HDL decreased significantly at the 4th, 6th, and 8th hours in patients with PAD and at the 6th hour in control subjects. The magnitude of postprandial lipemia, expressed as "the area under the incremental curve for TGs," was higher in patients with PAD than in control subjects (770 +/- 476 vs 391 +/- 195 mg/dL at 8 hours, P <.05). Multiple-regression analysis showed that baseline TGs were positively related to the magnitude of postprandial lipemia (P =.01) and that LDL size was negatively related (P =.05). CONCLUSIONS: This is the first documentation of postprandial behavior in patients with normolipemic PAD, suggesting the relevance of postprandial lipoprotein metabolism in the pathogenesis of peripheral atherosclerosis.
Authors: Patrik Hansson; Kirsten B Holven; Linn K L Øyri; Hilde K Brekke; Anne S Biong; Gyrd O Gjevestad; Ghulam S Raza; Karl-Heinz Herzig; Magne Thoresen; Stine M Ulven Journal: J Nutr Date: 2019-03-01 Impact factor: 4.798
Authors: R Scott Rector; Melissa A Linden; John Q Zhang; Shana O Warner; Thomas S Altena; Bryan K Smith; George G Ziogas; Ying Liu; Tom R Thomas Journal: J Clin Hypertens (Greenwich) Date: 2009-11 Impact factor: 3.738
Authors: Juan F Alcala-Diaz; Javier Delgado-Lista; Pablo Perez-Martinez; Antonio Garcia-Rios; Carmen Marin; Gracia M Quintana-Navarro; Purificacion Gomez-Luna; Antonio Camargo; Yolanda Almaden; Javier Caballero; Francisco J Tinahones; Jose M Ordovas; Francisco Perez-Jimenez; Jose Lopez-Miranda Journal: PLoS One Date: 2014-05-06 Impact factor: 3.240