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Delayed clearance of postprandial large TG-rich particles in normolipidemic carriers of LPL Asn291Ser gene variant.
J Lipid Res. 1999 Sep; 40(9):1663-70.JL

Abstract

The carrier frequency of Asn291Ser polymorphism of the lipoprotein lipase (LPL) gene is 4;-6% in the Western population. Heterozygotes are prone to fasting hypertriglyceridemia and low high density lipoprotein (HDL) cholesterol concentrations especially when secondary factors are superimposed on the genetic defect. We studied the LPL Asn291Ser gene variant as a modulator of postprandial lipemia in heterozygote carriers. Ten normolipidemic carriers were compared to ten control subjects, who were selected to have similar age, sex, BMI, and apolipoprotein (apo)E-phenotype. The subjects were given a lipid-rich mixed meal and their insulin sensitivity was determined by euglycemic hyperinsulinemic clamp technique. The two groups had comparable fasting triglycerides and glucose utilization rate during insulin infusion, but fasting HDL cholesterol was lower in carriers (1.25 +/- 0.05 mmol/L) than in the control subjects (1. 53 +/- 0.06 mmol/L, P = 0.005). In the postprandial state the most pronounced differences were found in the very low density lipoprotein 1 (VLDL1) fraction, where the carriers displayed higher responses of apoB-48 area under the curve (AUC), apoB-100 AUC, triglyceride AUC, and retinyl ester AUC than the control subjects. The most marked differences in apoB-48 and apoB-100 concentrations were observed late in the postprandial period (9 and 12 h), demonstrating delayed clearance of triglyceride-rich particles of both hepatic and intestinal origin. Postprandially, the carriers exhibited enrichment of triglycerides in HDL fraction. Thus, in normolipidemic carriers the LPL Asn291Ser gene variant delays postprandial triglyceride, apoB-48, apoB-100, and retinyl ester metabolism in VLDL1 fraction and alters postprandial HDL composition compared to matched non-carriers.

Authors+Show Affiliations

Division of Endocrinology and Diabetes, Department of Medicine, University of Helsinki, Haartmaninkatu 4, P.O. Box 340, FIN-00029 HUCH, Helsinki, Finland.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

10484613

Citation

Mero, N, et al. "Delayed Clearance of Postprandial Large TG-rich Particles in Normolipidemic Carriers of LPL Asn291Ser Gene Variant." Journal of Lipid Research, vol. 40, no. 9, 1999, pp. 1663-70.
Mero N, Suurinkeroinen L, Syvänne M, et al. Delayed clearance of postprandial large TG-rich particles in normolipidemic carriers of LPL Asn291Ser gene variant. J Lipid Res. 1999;40(9):1663-70.
Mero, N., Suurinkeroinen, L., Syvänne, M., Knudsen, P., Yki-Järvinen, H., & Taskinen, M. R. (1999). Delayed clearance of postprandial large TG-rich particles in normolipidemic carriers of LPL Asn291Ser gene variant. Journal of Lipid Research, 40(9), 1663-70.
Mero N, et al. Delayed Clearance of Postprandial Large TG-rich Particles in Normolipidemic Carriers of LPL Asn291Ser Gene Variant. J Lipid Res. 1999;40(9):1663-70. PubMed PMID: 10484613.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Delayed clearance of postprandial large TG-rich particles in normolipidemic carriers of LPL Asn291Ser gene variant. AU - Mero,N, AU - Suurinkeroinen,L, AU - Syvänne,M, AU - Knudsen,P, AU - Yki-Järvinen,H, AU - Taskinen,M R, PY - 1999/9/14/pubmed PY - 1999/9/14/medline PY - 1999/9/14/entrez SP - 1663 EP - 70 JF - Journal of lipid research JO - J. Lipid Res. VL - 40 IS - 9 N2 - The carrier frequency of Asn291Ser polymorphism of the lipoprotein lipase (LPL) gene is 4;-6% in the Western population. Heterozygotes are prone to fasting hypertriglyceridemia and low high density lipoprotein (HDL) cholesterol concentrations especially when secondary factors are superimposed on the genetic defect. We studied the LPL Asn291Ser gene variant as a modulator of postprandial lipemia in heterozygote carriers. Ten normolipidemic carriers were compared to ten control subjects, who were selected to have similar age, sex, BMI, and apolipoprotein (apo)E-phenotype. The subjects were given a lipid-rich mixed meal and their insulin sensitivity was determined by euglycemic hyperinsulinemic clamp technique. The two groups had comparable fasting triglycerides and glucose utilization rate during insulin infusion, but fasting HDL cholesterol was lower in carriers (1.25 +/- 0.05 mmol/L) than in the control subjects (1. 53 +/- 0.06 mmol/L, P = 0.005). In the postprandial state the most pronounced differences were found in the very low density lipoprotein 1 (VLDL1) fraction, where the carriers displayed higher responses of apoB-48 area under the curve (AUC), apoB-100 AUC, triglyceride AUC, and retinyl ester AUC than the control subjects. The most marked differences in apoB-48 and apoB-100 concentrations were observed late in the postprandial period (9 and 12 h), demonstrating delayed clearance of triglyceride-rich particles of both hepatic and intestinal origin. Postprandially, the carriers exhibited enrichment of triglycerides in HDL fraction. Thus, in normolipidemic carriers the LPL Asn291Ser gene variant delays postprandial triglyceride, apoB-48, apoB-100, and retinyl ester metabolism in VLDL1 fraction and alters postprandial HDL composition compared to matched non-carriers. SN - 0022-2275 UR - https://www.unboundmedicine.com/medline/citation/10484613/Delayed_clearance_of_postprandial_large_TG_rich_particles_in_normolipidemic_carriers_of_LPL_Asn291Ser_gene_variant_ L2 - http://www.jlr.org/cgi/pmidlookup?view=long&pmid=10484613 DB - PRIME DP - Unbound Medicine ER -