Abstract
The objective of the present study was to detect the association of the rs4731702 single nucleotide polymorphism (SNP) and serum lipid levels in the Guangxi Mulao and Han populations. A total of 727 subjects of Mulao and 740 subjects of Han Chinese were included. Serum low-density lipoprotein cholesterol (LDL-C) and apolipoprotein (Apo) B levels were higher in Mulao than in Han (P < 0.05). The T allele carriers had higher serum LDL-C and ApoAI levels in Mulao, whereas they had lower high-density lipoprotein cholesterol (HDL-C) levels and ratio of ApoAI to ApoB in Han (P < 0.05) than the T allele noncarriers. Subgroup analyses showed that the T allele carriers had higher HDL-C, LDL-C, and ApoAI levels in Mulao males and lower ApoAI levels and ratio of ApoAI to ApoB in Han males than the T allele noncarriers. The subjects with TT genotype in Han females also had higher total cholesterol, LDL-C, ApoAI, and ApoB levels than the subjects with CT or CC genotype. Serum lipid parameters were also correlated with several environmental factors in both ethnic groups. The differences in the association of KLF14 rs4731702 SNP and serum lipid levels between the two ethnic groups might partly result from different gene-environmental interactions.
Highlights
Cardiovascular diseases (CVD) are the leading causes of death in global populations, and the burden of CVD in terms of life-years lost, diminished quality of life, and direct and indirect medical costs is enormous [1]
The levels of Body mass index (BMI), diastolic blood pressure, and the ratio of ApoAI to ApoB were lower in Mulao than in Han (P < 0.05), whereas the levels of body height, low-density lipoprotein cholesterol (LDL-C), ApoB, and the percentages of subjects who consumed alcohol were higher in Mulao than in Han (P < 0.05–0.001)
After the genomic DNA of the samples was amplified by polymerase chain reaction (PCR) and imaged by 2.0% agarose gel electrophoresis, the purpose gene of 347 bp nucleotide sequences could be found in all samples (Figure 1)
Summary
Cardiovascular diseases (CVD) are the leading causes of death in global populations, and the burden of CVD in terms of life-years lost, diminished quality of life, and direct and indirect medical costs is enormous [1]. Epidemiological studies have consistently shown that dyslipidemia is a complex trait resulted from the joint effects of multiple genetic and environmental causes [7,8,9]. The heritability estimates of the interindividual variations in serum lipid levels from both twin and family studies are in the range of 40–70%, suggesting a considerable genetic contribution [10, 11]. Rare variants with large individual effects may contribute to the heritability of lipid traits [12]. Findings from large-scale studies suggested a strong linkage between the genetic variants at the Kruppel-like factor 14 (KLF14) locus and serum high-density lipoprotein cholesterol (HDLC) concentrations and type 2 diabetes [13,14,15,16,17,18].
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