Lipoprotein lipase variants associated with an endophenotype of hypertension: hypertension combined with elevated triglycerides

Chen, Pei; Jou, Yuh–Shan; Fann, Cathy S.J.; Chen, Jaw Wen; Chung, Chia Min; Lin, Chin Yu; Wu, Sheng Yeu; Kang, Mei Jyh; Chen, Ying Chuang; Jong, Yuh Shiun; Lo, Huey‐Ming; Kang, Chih Sen; Chen, Chien‐Chung; Chang, Huan Cheng; Huang, Nai Kuei; Wu, Yi; Pan, Wen Harn

doi:10.1002/humu.20812

Cited by 13 publications

(9 citation statements)

References 31 publications

(29 reference statements)

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“…In the young-onset hypertension example, in addition to confirming previous results [25] , the proposed method assesses gene-gene interactions between the estimated disease locus and SNP rs295. These findings can help investigators understand the underlying genetic mechanisms of a disease.…”

Section: Discussionmentioning

confidence: 69%

“…These estimated locations are consistent with the results of Chen el al. [25] . Since the non-parametric model is more robust against the one-locus assumption, the non-parametric approach obtained three additional estimates for with different initials: (i) 19.86076 cM, near SNP rs295, with a 95% CI = [19.86064, 19.86088]; (ii) 19.8634 cM, between SNPs rs320 and rs322, with a 95% CI = [19.86328, 19.86352], and (iii) 19.86522 cM, near SNP rs331 with a 95% CI = [19.86472, 19.86572].…”

Section: A Data Examplementioning

confidence: 99%

“…To illustrate the proposed method, the original, parametric, and non-parametric approaches were applied to a family-based hypertension study conducted at four community hospitals in northwestern Taiwan [25] . The sample of the study included a total of 88 young-onset hypertension trios from 66 families.…”

Section: A Data Examplementioning

confidence: 99%

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Incorporating Covariates into Multipoint Association Mapping in the Case-Parent Design

2010

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Background/Aims: To improve the efficiency of disease locus localization in association mapping using case-parent designs and to assess or account for the main covariate effects and gene-covariate interaction effects, while localizing the disease locus. Methods: The present study extends a multipoint fine-mapping approach to incorporate covariates into the association mapping of case-parent designs through parametric and non-parametric modeling. This approach is based on the expected preferential-allele-transmission statistics for transmission from either parent to an affected child. Results: Simulation studies indicate that the efficiency in estimating the disease locus increases considerably when incorporating a covariate associated with the disease. This is especially true when the genetic effect of the disease locus is small. The proposed approach was applied to a young-onset hypertension data sample. The relative efficiency of estimating the locus of young-onset hypertension increases 110-fold after incorporating triglyceride into the association mapping while localizing the disease variant in the lipoprotein lipase gene in the non-parametric model. By incorporating the information of SNP variants into the fine-mapping, the proposed method further assesses the gene-gene interactions between the SNP and the disease locus. Conclusion: With the incorporation of covariates, the proposed method cannot only improve efficiency in estimating disease loci, but can also elucidate the etiology of a complex disease.

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Section: Discussionmentioning

confidence: 69%

Section: A Data Examplementioning

confidence: 99%

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Incorporating Covariates into Multipoint Association Mapping in the Case-Parent Design

2010

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“…Gene mutations in lipoprotein lipase are reported to increase susceptibility for preeclampsia and endophenotype of HTN. 35,36 Polymorphism in the apolipoprotein C-III gene locus alters lipoprotein metabolism and can influence IR in essential hypertensive patients and increase the risk of CAD. 37,38 We suggest that genetic traits or individual variation in these enzymes may be associated with HTN, without affecting hypertriglyceridemia or IR, through environmental factors, such as life style differences.…”

Section: Resultsmentioning

confidence: 99%

Association of hypertension with small, dense low-density lipoprotein in patients without metabolic syndrome

Seo

Lee

et al. 2011

J Hum Hypertens

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A higher proportion of small, dense low-density lipoprotein (sdLDL) is known to be associated with a high prevalence of cardiovascular disease in association with metabolic syndrome (MS). Hypertension (HTN) is one of the known risk factors for MS. However, whether HTN is associated with sdLDL in patients without MS is not yet clear. The lipid profiles, including low-density-lipoprotein (LDL) subfractions, of 383 consecutive subjects were evaluated. The patients without MS consisted of 198 hypertensive patients (non-MS/HTN group) and 108 normotensive subjects (non-MS/non-HTN group). The peak and mean particle diameter of LDL were measured by gradient gel electrophoresis. Plasma total cholesterol, LDL cholesterol, high-density lipoprotein (HDL) cholesterol, triglyceride (TG), HDL cholesterol/Apo A1, LDL-C/ApoB and Apo(A1, B, CII and E) levels did not differ between the non-MS/non-HTN and non-MS/HTN groups. When analyzing LDL subfraction, the absolute amount of patterns A and B was not different between the non-MS/non-HTN and non-MS/HTN groups. Compared with the non-MS/non-HTN groups, the proportion of sdLDL was higher in the non-MS/HTN group (37.7% versus 39.9%, P ¼ 0.046), but not significant after adjustment of waist circumference, serum TG, age and statin usage. The proportion of sdLDL to total LDL was higher in hypertensive subjects, even those without MS, than in normotensive subjects. However, this difference of LDL subfraction in hypertensive patients is associated with higher waist circumference, higher serum TG, older age and more statin usage. This result suggests that HTN may contribute to atherosclerosis and endothelial dysfunction with associated risk factors that influence LDL size.

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“…Pleiotropic phenotypes indicate vulnerable DNA regions of insulin response elements as those are highly sensitive to hypertriglyceridemia and insulin promotor genes can modulate lipases and/or phospholipases [75]. Families can have favourable gene variants of apoproteins as healthy variants of apoB or of apoC3 reacting then about 39% lowering of postprandial triglycerides and 22% increase of HDL-cholesterol with 11% lowering of LDL-cholesterol compared to controls and these persons show 40% reduced prevalence of cardiovascular disorders [76] [77]. Other DNA regions encode variants of lipases/phospholipases and these regions are sensitive to triglyceride-related metabolic problems [78].…”

Section: Discussionmentioning

confidence: 99%

LDL-Related Intolerance to Glucose, Diastolic Hypertension and Additive Effects of Smoking Were Found with Three Female Study Groups

Korth¹

2016

Health

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Initial prodiabetic risk profiles were invented here with three female study groups consisting of primarily healthy women (A1: 1990-1999, n = 160; A2: 2009, n = 88; A: n = 248, 36 ± 14 years; B: 2014: n = 65, aged 37± 11 years). Significantly higher blood pressure was found comparing intolerance versus tolerance to glucose (p < 0.05, IGTT, 22 of 68). High LDL-cholesterol (LDL-C) showed additive effects as LDL-related intolerance was further related with rise of blood pressure (p < 0.05), of triglycerides (p = 0.02), of fasting blood glucose (p = 0.07) and of urine pathology (p = 0.07). High LDL-C of women who reported smoking at baseline was correlated with diastolic hypertension whereby alcohol problems overlapped (p = 0.036, A). Unhealthy combinations were found consisting of LDL-related intolerance to glucose, LDL-related smoking, of alcohol-related hypertriglyceridemia or of combined drinking and smoking testing urine pathology over the course of time. Obese women were at direct risk for hypertension in the presence of high LDL-C and submaximal ratio of serum albumin to triglycerides (Alb/Trig). Obese women reacted highly sensitive to critical alcohol consumption showing then macroalbuminuria. Current participants who disowned daily alcohol consumption showed healthy morning urines and normal fasting blood glucose. Mild decrease of HDL-C was observed during heavy smoking of relatively young women who had normal biomarkers. Women with intolerance to glucose were at direct risk for hypertension whereby high LDL-C and/or smoking triggered prodiabetic risk profiles. Obese women had elevated LDL-C during hypertension and reacted highly sensitive to alcohol-related proteinuria and/or hematuria. Keywords

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Lipoprotein lipase variants associated with an endophenotype of hypertension: hypertension combined with elevated triglycerides

Cited by 13 publications

References 31 publications

Incorporating Covariates into Multipoint Association Mapping in the Case-Parent Design

Incorporating Covariates into Multipoint Association Mapping in the Case-Parent Design

Association of hypertension with small, dense low-density lipoprotein in patients without metabolic syndrome

LDL-Related Intolerance to Glucose, Diastolic Hypertension and Additive Effects of Smoking Were Found with Three Female Study Groups

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