Lipoprotein and hepatic lipase gene variants in coronary atherosclerosis

Thorn, James A.; Chamberlain, John; Alcolado, John; Oka, Koichiro; Chan, Lawrence; Stocks, J.; Galton, D. J.

doi:10.1016/0021-9150(90)90182-i

Cited by 90 publications

(42 citation statements)

References 24 publications

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“…Peacock et al (28) also reported frequencies of 0.435 and 0.228 for PvuII(-) and HindIII(-), respectively, among 92 healthy control subjects. A strong linkage disequilibrium was also identified between the two PvuII and HindIII polymorphisms in several other studies (28)(29)(30)(31)(32)(33).…”

Section: Genotypes --------------------------------------------------supporting

confidence: 55%

Associations of three lipoprotein lipase gene polymorphisms, lipid profiles and coronary artery disease

et al. 2013

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Abstract. Lipoprotein lipase (LPL) plays a central role in lipoprotein metabolism by hydrolyzing the core triglycerides (TGs) of circulating chylomicrons and very-low-density lipoprotein (VLDL). The effects of LPL polymorphisms on lipid levels and coronary artery disease (CAD) have been inconsistent among studies and populations. To assess the lipid profiles and distributions of three LPL gene polymorphisms in Saudi patients with CAD, the HindIII, PvuII and Ser447Ter polymorphisms in the LPL gene were analyzed in 226 patients with CAD and 110 controls. Polymerase chain reaction-restriction fragment length polymorphism was used to detect LPL gene polymorphisms. The plasma lipid profiles of the patients were determined using standard enzymatic methods. Patients in the CAD group had significantly higher triglyceride (TG), total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) levels than controls irrespective of the HindIII, PvuII or Ser447Ter genotype. Compared to the findings in controls, the HindIII TT, PvuII TC and Ser447Ter CC genotypes were associated with significantly reduced high-density lipoprotein cholesterol (HDL-C) levels in patients with CAD (P<0.0001). In summary, there are associations between LPL gene variants and high plasma TG, TC and LDL-C levels as well as low HDL-C levels.

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Section: Genotypes --------------------------------------------------supporting

confidence: 55%

Associations of three lipoprotein lipase gene polymorphisms, lipid profiles and coronary artery disease

et al. 2013

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“…22,23 In fact, the 447stop allele has been reported to be associated with higher HDL cholesterol and lower serum triglyceride levels, thus resulting in a lower risk of coronary artery and aterothrombotic cerebral diseases. 7,8,19 The mechanism by which the 447stop allele enhances the pathway of carcinogenesis in the prostate cell remains unknown. The activated free fatty acid released by LPL is hydrolyzed and then metabolized to acetyl CoA and NADH.…”

Section: Discussionmentioning

confidence: 99%

“…These polymorphisms have been shown to underlie changes in plasma lipoprotein levels and to be one of the important risk factors for cardiovascular diseases. [7][8][9] However, no information is available on the relationship between these LPL polymorphisms and prostate cancer risk.…”

mentioning

confidence: 99%

Association of lipoprotein lipase gene polymorphism with risk of prostate cancer in a japanese population

Narita

Tsuchiya

Wang

et al. 2004

Intl Journal of Cancer

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Prostate cancer has a prominent variation in incidence among different racial/ethnic groups. Previous studies have demonstrated that nutritional factors, especially fat intake, may contribute to the development and progression of prostate cancer. In fact, animal studies have shown that lower fat intake inhibits prostate cancer growth. 1,2 Giovannucci et al. 3 have demonstrated a marked increase in the likelihood of prostate cancer in men with a high fat intake from red meat and a significant association between the total intake of essential fatty acids such as ␣-linolenic acid and the development of aggressive prostate cancer. On the other hand, the significance of genetic factors in the development and progression of prostate cancer has been well documented. While the incidence of prostate cancer in the native Japanese population is 5 times lower than that in Caucasians, Japanese Americans have an approximately 40 -50% higher rate of prostate cancer than Japanese men, but the rate of prostate cancer in Japanese American men does not appear to approach that of Caucasians. 4,5 These reports further support the concept that genetic factors in combination with dietary factors may have a significant impact on susceptibility to prostate cancer. In exploring genetic susceptibility factors for prostate cancer, a population whose nutritional or environmental factors are small may be an ideal cohort, in which individual differences in such factors and gene-environment interactions are minimized. It has been reported that the calorie intake and the proportion of fat to total calories consumed are quite low in Japan compared to those in Western countries. 6 Therefore, the Japanese might be an ideal population to investigate the association between polymorphisms and prostate cancer risk because the nutritional factors may be minimized.Lipoprotein lipase (LPL) plays a crucial role in fat metabolism. LPL hydrolyses triglycerides in both chylomicrons and very-lowdensity lipoproteins (VLDLs) and liberates free fatty acids. The human LPL gene is localized to chromosome 8p22. The gene contains 10 exons and has several DNA variants designated as Ser447stop, HindIII and PvuII polymorphisms. These polymorphisms have been shown to underlie changes in plasma lipoprotein levels and to be one of the important risk factors for cardiovascular diseases. 7-9 However, no information is available on the relationship between these LPL polymorphisms and prostate cancer risk.In this study, with the hypothesis that the LPL polymorphisms may be associated with the onset and/or progression of prostate cancer, we analyzed the LPL genotype of patients with prostate cancer or benign prostatic hyperplasia (BPH) as compared with male controls in a native Japanese population. MATERIAL AND METHODS SubjectsA total of 708 subjects consisting of 273 prostate cancer patients, 205 BPH patients and 230 male controls who visited Akita University Medical Center, its related community hospitals and Kyoto University Hospital were enrolled in this study. Because thi...

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“…Although the P 2 allele was independently associated with microalbuminuria, it is worth noting that LPL variants have previously been shown to correlate with development and severity of coronary artery disease [24,25,26,33], hence the association of P 2 with MA could, in part, be derived from the independent relationship of LPL genotypes and microalbuminuria with cardiovascular disease.…”

Section: Resultsmentioning

confidence: 96%

“…We and others have previously found that genetic variants of LPL relate to dyslipidaemia and atherosclerosis, including concentrations of triglycerides [24,25,26,27,28,29], high density lipoprotein cholesterol (HDL-C) [24,25,30,31,32], and total cholesterol [25,29,31], development [24,25,33] and severity [24,26] of coronary artery disease, familial combined hyperlipidaemia [34,35] and familial chylomicronaemia [36]. Recently, no relationship was found between an exonic LPL polymorphism and Type I diabetic nephropathy [37], although a potent effect of total cholesterol, triglycerides and apo-B was noted on DN.…”

mentioning

confidence: 96%

Lipoprotein lipase gene variants relate to presence and degree of microalbuminuria in Type II diabetes

et al. 2002

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Aims/hypothesis. Lipids and lipoproteins, particularly triglyceride rich lipoproteins, could influence the development and progression of microalbuminuria in diabetes. Lipoprotein lipase gene variants have been found to correlate with lipid/lipoprotein concentrations, especially hypertriglyceridaemia. We assessed the influence of this gene on microalbuminuria in Type II (insulin-dependent) diabetes mellitus. Methods. Microalbuminuria was determined quantitatively in 386 sequential Type II diabetic patients by measurement of the albumin-to-creatinine ratio (ACR). DNA was analysed for two common intronic LPL single nucleotide polymorphisms (Pvu II, intron 6, and Hind III, intron 8), and three common exonic mutations (Asp 9 -Asn, exon 2, Asn 291 -Ser, exon 6, and Ser 447 -Ter, exon 9). Results. Individuals with P 2 P 2 (Pvu II) and H 2 H 2 (Hind III) genotypes had significantly greater ACRs (P 2 P 2 vs P 1 P 1 +P 1 P 2 , 5.0±0.5 vs 3.4±0.3, p=0.0004 and H 2 H 2 vs H 1 H 1 +H 1 H 2 , 4.3±0.4 vs 3.4±0.3, p=0.04). Logistic regression analysis demonstrated that only the P 2 P 2 genotype (p=0.0004), systolic BP (p=0.008) and creatinine (p=0.031) were independently associated with the presence of microalbuminuria/proteinuria. P 2 homozygotes were 170% more likely to have microalbuminuria or proteinuria, O.R. 2.7 (1.6-4.5, p=0.0001), 150% more likely to have microalbuminuria, O.R. 2.5 (1.5-4.3, p=0.001), and 330% more likely to have proteinuria, O.R. 4.3 (1.6-11.4, p=0.004). There were no associations of microalbuminuria with any of the exonic polymorphisms. Conclusion/interpretation. Genetic variants of lipoprotein lipase correlate with presence and severity of microalbuminuria in Type II diabetes, independent of effect on serum lipids. This association is only apparent in genetic variants demonstrating greatest heterozygosity. [Diabetologia (2002) 45:905-913]

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Lipoprotein and hepatic lipase gene variants in coronary atherosclerosis

Cited by 90 publications

References 24 publications

Associations of three lipoprotein lipase gene polymorphisms, lipid profiles and coronary artery disease

Associations of three lipoprotein lipase gene polymorphisms, lipid profiles and coronary artery disease

Association of lipoprotein lipase gene polymorphism with risk of prostate cancer in a japanese population

Lipoprotein lipase gene variants relate to presence and degree of microalbuminuria in Type II diabetes

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