Influence of common variants in the CETP, LPL, HL and APO E genes on LDL heterogeneity in healthy, middle-aged men

Skoglund‐Andersson, C.; Ehrenborg, Ewa; Fisher, Rachel M.; Olivecrona, Gunilla; Hamsten, Anders; Karpe, Fredrik

doi:10.1016/s0021-9150(03)00016-9

Cited by 48 publications

(36 citation statements)

References 33 publications

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“…There were no homozygotes and no compound LPL heterozygotes in our study sample. The S447X variant, associated with an increased enzymatic activity and a putative protective effect on lipid homeostasis for G allele carriers (Skoglund-Andersson et al 2003;van Bockxmeer et al 2001), was analyzed alone, and there were no differences between controls (allele frequency = 12.1%) and cases (allele frequency = 10.2%) ( Table 4).…”

Section: Lpl Genotypesmentioning

confidence: 99%

The combination of ApoCIII, hepatic lipase and hormono sensitive lipase gene polymorphisms suggests an association with susceptibility to gestational hypertension

et al. 2007

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Dyslipidemia and insulin resistance contribute to the endothelial cell dysfunction in hypertensive disorders of pregnancy (HDP) and increase the long-term risk of cardiovascular disease (CVD). The genes linking susceptibility to gestational hypertension (GH) and/or preeclampsia (PE) to the long-term risk of CVD are still unknown. We evaluated the potential association between 14 polymorphisms from six genes involved in lipid metabolism and insulin action and the risk of HDP: namely the lipoprotein lipase (LPL), hepatic lipase (LIPC), hormone sensitive lipase (LIPE), cholesteryl ester transfer protein (CETP), ApoCIII and ApoE gene polymorphisms. Overall, 169 women with HDP [proteinuria (PE) and gestational hypertension without proteinuria (GH)] and 169 controls matched for age and year of delivery were genotyped. Homozygosity of the -514T allele of the -514C > T polymorphism (LIPC gene) decreased the risk of GH (OR = 0.17, CI 95 : 0.02-0.76), while there were more -60G carriers of the -60C > G LIPE gene polymorphism (OR = 3.51, CI 95 :1.02-12.10) among GH cases, but not in PE cases. The common ApoCIII two-locus -482CC/3238CC genotype was lower in women with GH compared with controls (OR = 0.53, CI 95 : 0.3-0.9). The combined frequency of at-risk genotypes was higher in cases of GH compared with controls [one at-risk genotype: OR = 3.38 (95% CI: 0.48-41.8); two or more at-risk genotypes: OR = 7.14 (95% CI: 1.21-92.3, P = 0.01)], suggesting a gene-dose effect. We conclude that the combined effect of LIPC, LIPE and ApoCIII gene polymorphisms may increase the likelihood of GH, but seemingly not of PE.

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Section: Lpl Genotypesmentioning

confidence: 99%

The combination of ApoCIII, hepatic lipase and hormono sensitive lipase gene polymorphisms suggests an association with susceptibility to gestational hypertension

et al. 2007

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“…However, the same trend was observed in men and women for higher LDL type from the 2 to 4 subjects. The lowering effect of the 4 allele was confirmed in Japanese subjects (84) and in men of North European descent (85), showing that carriers of this allele had smaller LDL particle size than those without the 4 allele. Consistent with these observations, Haffner et al (86) demonstrated a progressive decrease in LDL size in both men and women from apoE2/3, apoE3/ 3, and apoE3/4 genotypes.…”

Section: Association Studiesmentioning

confidence: 81%

“…However, a larger study, conducted in 2,667 subjects participating in the Framingham Offspring Study, found no relationship between HL polymorphism at position Ϫ514 and the LDL particle size measured by GGE (95). This lack of association between this variant and LDL size measured by GGE was also observed in a subgroup of unrelated subjects from FCHL Dutch families (78) and in a cohort of healthy, middle-aged men (85). The different methods used to characterize LDL particles might explain the inconsistency.…”

Section: Association Studiesmentioning

confidence: 97%

“…The latter study also reported no association between LDL size and a third gene variant in linkage disequilibrium with the Taq1B polymorphism named Ϫ629CϾA. In contrast, carriers of the Ϫ629CϾA polymorphism had increased LDL-PPD compared with CETP-629C homozygotes in a cohort of healthy, middle-aged men (85). Finally, a less frequent missense mutation, D442G in exon 15, in the CETP gene was investigated in patients with CAD.…”

Section: Association Studiesmentioning

confidence: 97%

“…Hokanson et al (77) confirmed the LDL size-reducing effect of LPL deficiency in five families with structural mutations in the LPL gene. Subsequently, the Ser447-Ter mutation in exon 9 was associated with larger LDL size (85,108). This mutation causes a premature termination codon that, surprisingly, increases the enzymatic activity of LPL (85,109).…”

Section: Association Studiesmentioning

confidence: 99%

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Genetics of LDL particle heterogeneity

Bossé

Pérusse

Vohl

2004

Journal of Lipid Research

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Effects of fluvastatin slow-release (xl 80 mg) versus simvastatin (20 mg) on the lipid triad in patients with type 2 diabetes

et al. 2005

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The lipid triad is the association of small, dense (sd) low-density lipoprotein (LDL), low high-density lipoprotein (HDL), and hypertriglyceridemia, all of which play a role in coronary artery disease in patients with type 2 diabetes. Although statins have demonstrated clear positive effects on cardiovascular morbidity/mortality in patients with diabetes and on single components of the lipid triad, it remains controversial whether they affect all components of the triad in these patients. Therefore, we performed a single-center, parallel-group, prospective, randomized, open-label, blinded-endpoint (PROBE)-type comparison of fluvastatin extended-release (XL) 80 mg (n=48) and simvastatin 20 mg (n=46), each given once daily for 2 months to patients with type 2 diabetes with the lipid triad, who were enrolled after a 1-month lifestyle modification and dietary intervention program. After fluvastatin therapy, LDL (-51%; P<.01), apolipoprotein B (ApoB; -33%; P<.01), intermediate-density LDL (idLDL) (-14.3%; P<.05), sdLDL (-45%; P<.01), and triglycerides (-38%; P<.01) were significantly decreased, and HDL (+14.3%; P<.05) and apolipoprotein A-I (ApoA-I; +7%; P<.05) were increased; large buoyant (lb) LDL did not change (P=NS). Simvastatin therapy decreased LDL (-55.1%; P<.01), ApoB (-46%; P<.01), lbLDL (-33.3%; P<.05), idLDL (-22.7%; P<.05), sdLDL (-33.3%; P<.05), and triglycerides (-47.9%; P<.01); HDL was not changed (P=NS) after simvastatin, but ApoA-I was increased (+11.3%; P<.01). HDL increases (P<.01) and sdLDL decreases (P<.01) were significantly greater after fluvastatin compared with simvastatin therapy; LDL, triglycerides, ApoB, and idLDL changes were similar after both therapies (P=NS), and lbLDL decreases were greater with simvastatin therapy (P<.05). With both treatments, classic mean LDL and ApoB target levels were achieved in most patients. We conclude that the lipid triad can be controlled with fluvastatin XL 80 mg in patients with type 2 diabetes.

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Influence of common variants in the CETP, LPL, HL and APO E genes on LDL heterogeneity in healthy, middle-aged men

Cited by 48 publications

References 33 publications

The combination of ApoCIII, hepatic lipase and hormono sensitive lipase gene polymorphisms suggests an association with susceptibility to gestational hypertension

The combination of ApoCIII, hepatic lipase and hormono sensitive lipase gene polymorphisms suggests an association with susceptibility to gestational hypertension

Genetics of LDL particle heterogeneity

Effects of fluvastatin slow-release (xl 80 mg) versus simvastatin (20 mg) on the lipid triad in patients with type 2 diabetes

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