Lipoprotein Lipase Gene Polymorphisms Research Articles

HINDIII AND S447X POLYMORPHISMS OF LIPOPROTEIN LIPASE GENE AND THEIR RELATIONSHIP TO CORONARY ARTERY DISEASE

Coronary artery disease (CAD) is a leading cause of morbidity and mortality worldwide. Lipoprotein lipase is a key enzyme in lipoprotein metabolism and its gene is a major candidate gene for coronary heart disease. The aim of the present work was to study the association of HindIII and S447X polymorphisms in lipoprotein lipase gene with coronary artery disease and their impact on lipid metabolism. The study was conducted on 60 patients with CAD as defined by coronary angiography in addition to 50 apparently healthy subjects serving as a control group. Lipoprotein lipase gene polymorphism (HindIII and S447X) detection was done by polymerase chain reaction– restriction fragment length polymorphism (PCR- RFLP) technique. The present study revealed that the studied population was in Hardy- Weinberg equilibrium (HWE). HindIII polymorphism frequency did not differ between patients and controls. Meanwhile, the S447X polymorphism (SX genotype and the X allele) was more frequent in controls as compared to CAD patients. Carriers of X allele and H-X haplotype had lower triglyceride levels and higher HDL-C levels as compared to those with absent X allele and H+S haplotype. Meanwhile H- allele was not associated with any change in lipid profile. In conclusion, the S447X polymorphism can be considered as one of the protective factors against development of CAD. Meanwhile, HindIII polymorphism failed to prove any association with CAD. Keywords : Coronary artery disease; lipoprotein lipase; HindIII polymorphism; S447X polymorphism; PCR; RFLP

Association of the HindIII Lipoprotein Lipase Gene Polymorphism with the Development of the Non-Biliary Acute Pancreatitis: a Pilot Study.

We studied the relationship between lipoprotein lipase (LPL) gene HindIII polymorphism and the development of acute pancreatitis in the Russian population. Whole blood samples were collected from 145 patients with acute non-biliary pancreatitis and 191 healthy individuals. Genotyping of LPL gene HindIII (rs320) polymorphism was performed by PCR with TaqMan assay. It was found that allele H+ (OR=0.63, 95%CI 0.41-0.96, p=0.03) and genotype H+/H+ (OR=1.79, 95%CI 1.06-3.04, p=0.03) were associated with the risk of acute non-biliary pancreatitis only in males. In this study, the relationship between HindIII polymorphism of LPL gene with the risk of acute non-biliary pancreatitis was revealed.

Impact of Lipoprotein Lipase Gene Polymorphism, S447X, on Postprandial Triacylglycerol and Glucose Response to Sequential Meal Ingestion.

Lipoprotein lipase (LPL) is a key rate-limiting enzyme for the hydrolysis of triacylglycerol (TAG) in chylomicrons and very low-density lipoprotein. Given that postprandial assessment of lipoprotein metabolism may provide a more physiological perspective of disturbances in lipoprotein homeostasis compared to assessment in the fasting state, we have investigated the influence of two commonly studied LPL polymorphisms (rs320, HindIII; rs328, S447X) on postprandial lipaemia, in 261 participants using a standard sequential meal challenge. S447 homozygotes had lower fasting HDL-C (p = 0.015) and a trend for higher fasting TAG (p = 0.057) concentrations relative to the 447X allele carriers. In the postprandial state, there was an association of the S447X polymorphism with postprandial TAG and glucose, where S447 homozygotes had 12% higher TAG area under the curve (AUC) (p = 0.037), 8.4% higher glucose-AUC (p = 0.006) and 22% higher glucose-incremental area under the curve (IAUC) (p = 0.042). A significant gene–gender interaction was observed for fasting TAG (p = 0.004), TAG-AUC (Pinteraction = 0.004) and TAG-IAUC (Pinteraction = 0.016), where associations were only evident in men. In conclusion, our study provides novel findings of an effect of LPL S447X polymorphism on the postprandial glucose and gender-specific impact of the polymorphism on fasting and postprandial TAG concentrations in response to sequential meal challenge in healthy participants.

Association studies on the bovine lipoprotein lipase gene polymorphism with growth and carcass quality traits in Qinchuan cattle

Lipoprotein lipase (LPL) is considered as an essential enzyme in lipid deposition and tissue metabolism. It has been proposed to be a lead candidate gene for genetic markers of lipid deposition and energy balance. In this paper, polymorphisms in the LPL gene were investigated in 554 Chinese Qinchuan cattle by PCR-RFLP and DNA sequencing. Seven single nucleotide polymorphisms (SNPs) were identified, which included one mutation (g.91C > T) in the 5′untranslated region (UTR), four synonymous mutations (g.17015A > G, g.18362G > A, g.18377T > C and g.19873T > C) and two mutations (g.25225A > G and g.25316T > G) in the 3′UTR. The frequencies of SNP g.18377T > C and g.25316T > G were skewed from Hardy–Weinberg equilibrium in all the samples (chi-square test, P < 0.05). An association analysis showed that five loci (except for g.91C > T and g.18377T > C) were significantly correlated with some growth and carcass quality traits. These results demonstrate that LPL might be a potential candidate gene for marker-assisted selection (MAS).

RETRACTED: Association between peroxisome proliferator-activated receptor, UCP3 and lipoprotein lipase gene polymorphisms and obesity in Chinese adolescents

This article has been retracted: please see Elsevier Policy on Article Withdrawal (http://www.elsevier.com/locate/withdrawalpolicy). Please note that this retraction notice has been updated in September 2021, as follows: This article has been retracted at the request of the Editors in Chief due to concerns regarding the authorship. Certain individuals were erroneously indicated as co-authors of the article when it was originally published. These individuals have informed the journal that they did not contribute to the article and that they had no knowledge of its submission for publication. We confirm, following investigation, that those individuals previously identified by the submitting author as co-authors did not author, approve or submit this article for publication, and the previous attribution of the article to them was in error. We have not had a response from Dr Mao and Dr Cai regarding authorship. As a result of the correspondence with Associate Professor Z. Zou and Dr L. Wang, we believe that the paper needs to be retracted and have elected to proceed with retraction.

Research on the prevalence of two polymorphisms of lipoprotein lipase gene in patients with metabolic syndrome

Research on the prevalence of two polymorphisms of lipoprotein lipase gene in patients with metabolic syndrome

Relationship between a lipoprotein lipase gene polymorphism in placental tissue and insulin resistance in patients with gestational diabetes mellitus

The aim of this study was to investigate the relationship between a lipoprotein lipase (LPL) gene polymorphism in placental tissue and insulin resistance (IR) in patients with gestational diabetes mellitus. Using polymerase chain reaction-restriction enzyme fragment length polymorphism (PCR-RFLP) analysis, the LPL HindIII RFLP was examined in the placental tissue of 110 patients with gestational diabetes mellitus (observation group) and 110 women with normal gestation (control group). The relationships between fasting plasma glucose (FPG), postprandial plasma glucose (PPG), fasting insulin (FINS), cholesterol (TC), triglyceride (TG), high density lipoprotein (HDL), low density lipoprotein (LDL), body mass index (BMI), and IR indices and the LPL polymorphism in the two study groups and their offspring were determined. The frequency of the H+ allele was significantly higher in the observation group than in the controls (P < 0.05). There were statistically significant differences in the observation group between the FPG, PPG, LDL, TC, TG, HDL, BMI, FINS, and IR indices of the H+H+ group and those of the non H+H+ type patients (P < 0.05). Correlation analysis showed that the LPL gene polymorphism was positively related to IR. There were statistically significant differences between HDL, BMI, and IR indices between the two study groups (P < 0.05). In conclusion, the LPL gene polymorphism was determined to be the main factor related to IR in women with gestational diabetes, and was also found to be related to the IR of their offspring.

The hindIII polymorphism of lipoprotein lipase gene and lipid profile in caucasian population of west siberia

Objectives: We have analyzed the frequencies of HindIII polymorphism of lipoprotein lipase gene (LPL) and lipid profile in Caucasian population of West Siberia and the groups this high and low total cholesterol (TC) level.

Association of lipoprotein lipase gene polymorphisms with lipid profiles in atherosclerotic coronary artery disease

BackgroundCoronary artery disease (CAD) is a complex disease with well-documented genetic and environmental components. Lipoprotein lipase (LPL) is considered a potential target as the variations in the LPL gene have been implicated in a number of pathophysiologic conditions associated with CAD.ObjectivesThe aims of this study were to determine the relationship between LPL gene polymorphisms (PvuII and S447X) and lipid profiles in patients with CAD, and to determine its role in the prediction of the severity of coronary atherosclerosis.Patients and methodsA total of 100 individuals were classified by coronary angiography: 80 patients with CAD and 20 controls (normal coronary angiography). Clinical data, carotid sonography, blood lipid profiles, and LPL genotyping for PvuII and S447X using PCR-RFLP were assessed.ResultsPlasma lipid profiles and carotid intima-media thickness were significantly increased in CAD patients compared with controls. LPL polymorphisms were distributed for PvuII genotypes and alleles in CAD patients versus controls as follows: CC (2.5 vs. 15%), CT (76.25 vs. 75%), and TT (21.25 vs. 10.0%) genotypes; T (59.4 vs. 47.5%) and C (40.6 vs. 52.5%) alleles. LPL S447X genotypes and alleles showed no significant difference between CAD and controls. CT genotypes of LPL PvuII were the highest in number and percentage compared with CC and TT among the CAD patients (P<0.05). However, there was a significant decrease in the systolic and diastolic velocity in CC versus CG genotypes of S447X among CAD patients (P < 0.05). Other carotid ultrasound, lipid profiles, or coronary angiography parameters were not significant in both genotypes of LPL among CAD patients.ConclusionAtherosclerotic ischemic patients showed a higher association in the number and percent of CT genotypes of PvuII LPL that may be an important diagnostic risk biomarker and may implicate a therapeutic intervention in CAD.

Lipoprotein Lipase and PPAR Alpha Gene Polymorphisms, Increased Very-Low-Density Lipoprotein Levels, and Decreased High-Density Lipoprotein Levels as Risk Markers for the Development of Visceral Leishmaniasis byLeishmania infantum

In visceral leishmaniasis (VL) endemic areas, a minority of infected individuals progress to disease since most of them develop protective immunity. Therefore, we investigated the risk markers of VL within nonimmune sector. Analyzing infected symptomatic and, asymptomatic, and noninfected individuals, VL patients presented with reduced high-density lipoprotein cholesterol (HDL-C), elevated triacylglycerol (TAG), and elevated very-low-density lipoprotein cholesterol (VLDL-C) levels. A polymorphism analysis of the lipoprotein lipase (LPL) gene using HindIII restriction digestion (N = 156 samples) (H+ = the presence and H− = the absence of mutation) revealed an increased adjusted odds ratio (OR) of VL versus noninfected individuals when the H+/H+ was compared with the H−/H− genotype (OR = 21.3; 95% CI = 2.32–3335.3; P = 0.003). The H+/H+ genotype and the H+ allele were associated with elevated VLDL-C and TAG levels (P < 0.05) and reduced HDL-C levels (P < 0.05). An analysis of the L162V polymorphism in the peroxisome proliferator-activated receptor alpha (PPARα) gene (n = 248) revealed an increased adjusted OR when the Leu/Val was compared with the Leu/Leu genotype (OR = 8.77; 95% CI = 1.41–78.70; P = 0.014). High TAG (P = 0.021) and VLDL-C (P = 0.023) levels were associated with susceptibility to VL, whereas low HDL (P = 0.006) levels with resistance to infection. The mutated LPL and the PPARα Leu/Val genotypes may be considered risk markers for the development of VL.

Analysis of the association Hind III Polymorphism of Lipoprotein Lipase gene on the risk of coronary artery disease

Background and Aim: Coronary artery disease (CAD) is one of the leadin g causes of death and disability around the world. In teraction between genetic and environmental factors determines susceptibility of an individual to develop coronary artery disease. Lipoprotein lipase (LPL) play an important role in the metabolism of HDL-C (High Density Lipoprotein Cholesterol), LDL-C (Low Density Lipoprotein Cholesterol) and triglycerides (TG). Dysfunction of LPL as a result of genetic variants of lipoprotein lipase ge ne is associated with increased risk of CAD. The aim of the present study was to in vestigate the relationship between the risk of coronary artery disease and LDL -C, HDL-C and TG (triglycerides) levels by lipoprotein lipase gene Hind III polymorphism. Methods: A total of 202 subjects including 114 patients with coronary artery disease and 88 control participated in this study. The Hind III polymorphism of the lipoprotein lipase gene was determined by PCR- RFLP (Polymerase Chain Reaction-Restriction Fragment Length Polymorphism). In the presence and absence of restriction site, the genotypes are desc ribed H+/+, H-/- respectively. Results: In this survey, a significant association between the frequent H+/+ genotype and unfavorable TG levels was observed in our population. For the Hind III genotypes, within the healthy subjects (n=88), the H+/+ genotype was found in 67 individuals (58.8%), H-/+ genotype in 38 individuals (33.3%), and 9 individuals (7.8%) carried the H-/- genotype. Within the CAD group (n=114), 47 individuals (53.4%) with H+/+ genotype, 36 (41%) with H-/+ genotype, and 5 (5.6%) carried the H-/- genotype. Conclusion: There was no significant difference between the di stribution of LPL- Hind III genotypes and the healthy subjects and the patient s with CAD (P<0.05, 0. 645). The study of LPL genotypes confirms the exist ence of interrelations between TG levels (P<0.05), but this polymorphisms were not detected as independent risk factors for CAD (P<0.05).

A Lipoprotein Lipase Gene Polymorphism Interacts with Consumption of Alcohol and Unsaturated Fat to Modulate Serum HDL-Cholesterol Concentrations1–3

There are limited data from prospective studies regarding interactions between lipoprotein lipase gene (LPL) and lifestyle factors in association with HDL-cholesterol (HDL-C) concentrations, a biomarker of coronary heart disease risk. Our prospective cohort study investigated the interactive effects of a common LPL polymorphism and lifestyle factors, including obesity, smoking, alcohol consumption, physical activity, and dietary intake, on follow-up measurements of HDL-C and triglyceride (TG) concentrations. A total of 5314 Korean men and women aged 40–69 y participated in the study. Serum HDL-C and TG concentrations were measured in all participants at baseline and 6-y follow-up examinations. On the basis of genome-wide association data for HDL-C and TG concentrations, we selected the most significant polymorphism (rs10503669), which was in high linkage disequilibrium with the serine 447 stop (S447×) mutation (D′ = 0.99) of LPL. We found that carrying the T allele reflecting the LPL ×447 allele was positively associated with follow-up measurement of HDL-C concentrations (P < 0.001). In the linear regression model adjusted for baseline HDL-C concentration and potential risk factors, we observed interactive effects of the polymorphism and consumption of alcohol (P-interaction < 0.01) and unsaturated fat (P-interaction < 0.05) on follow-up measurement of HDL-C concentrations. We also observed interactive effects of the polymorphism and body mass index (P-interaction < 0.01) on follow-up measurement of TG concentrations after adjusting for the baseline level and potential risk factors. Our findings suggest that carriers of the LPL ×447 allele benefit from moderate alcohol consumption and a diet high in unsaturated fat to minimize reduction of blood HDL-C concentrations and that obese persons who do not carry the LPL ×447 allele need to control body weight to prevent hypertriglyceridemia.

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

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.

Synergistic Effect Between Lipoprotein Lipase and Apolipoprotein C3 Genes in Determining the Severity of Coronary Artery Disease

A number of genetic variants have been identified in the lipoprotein lipase (LPL) gene. We aimed to investigate the possible associations between LPL gene and apolipoprotein C3 (APOC3) gene polymorphisms with coronary artery disease (CAD) and its severity, as well as the interaction between these polymorphisms and classical risk factors. The HindIII variant of LPL and APOC3 were genotyped in 156 CAD patients and 154 subjects as a control group. We found that the odds ratio (OR) estimating the effect of joint exposure to H2H2 genotype of LPL and S2S2 genotype of APOC3 was significantly higher than the OR estimating the effect of each factor in the absence of the other. The present study points to a synergistic interaction between H2H2 genotype of LPL gene and S2S2 genotype of APOC3 gene that leads to increased severity of CAD. Smoking, low HDL, and diabetes increased the severity of CAD in patients carrying these risky genotypes.

Impact of Lipoprotein Lipase Gene Polymorphisms on Severity of Coronary Artery Disease

Impact of Lipoprotein Lipase Gene Polymorphisms on Severity of Coronary Artery Disease

Genetic polymorphisms of lipoprotein lipase gene and their associations with growth traits in Xiangxi cattle

Lipoprotein lipase (LPL), involved in the metabolism and transport of lipids, regulate energy balance, fat deposition and growth traits. The objective of this study was to investigate the single nucleotide polymorphisms (SNPs) of LPL gene and to determine their associations between these polymorphisms and growth traits in Xiangxi cattle breed. In this study, six novel SNPs (C355157T, T355169C, T355186G, A355210G, T355348A and T355420C) and one reported SNP (A355427T, has been recorded in dbSNP, ID rs110590698) were detected using polymerase chain reaction and DNA sequencing method. Genotyping and genetic diversity analysis were performed in 240 Xiangxi cattle on the basis of sequence alignment, which indicated that five SNPs (C355157T, 355186G, T355348A, T355420C, A355427T) were in abundant genetic diversity, and the other two SNPs (T355169C and TA355210G) were in low genetic diversity. Linkage disequilibrium analysis showed that 18 different haplotypes were identified in these animals. Moreover, the results of the association between LPL gene polymorphisms and growth traits indicated that the individuals with H1H1 haplotype combination had higher BW and HG than those with other haplotype combinations (P < 0.05). The animals with CC genotype maintain higher mean values for BW than those with the CT and TT genotypes (P < 0.05) at T355420C locus. The animals with the AA genotype have lower mean values for WH, BL, HG and BW than those with the AT and TT genotypes at A355427T locus (P < 0.05). The results suggested that the SNPs of the LPL gene might be useful genetic markers for growth traits in the bovine reproduction and breeding.

Six lipoprotein lipase gene polymorphisms, lipid profile and coronary stenosis in a Tunisian population

Lipoprotein lipase (LPL) is the rate-limiting enzyme in the hydrolysis of triglyceride-rich lipoprotein particles (Chylomicrons and very-low-density lipoprotein). LPL polymorphisms' effects on lipids and coronary artery disease are controversial among studies and populations. Our aim was to study the association between six polymorphisms, haplotypes and significant coronary stenosis (SCS), disease severity and lipid parameters in Tunisian patients. LPL PvuII, 93 T/G, 188 G/E, HindIII, N291S and D9N polymorphisms were analyzed in 316 patients who underwent coronary angiography. Assessment of coronary angiograms identified SCS as the presence of stenosis >50 % in at least one major coronary artery. The stenosis severity was determined by using Gensini score and vessels number. A significant association of SCS with TT of the HindIII polymorphism was showed (odds ratio (OR): 2.84, 95 % CI, 1.19-7.40, p = 0.017) and TG (OR: 1.77, 95 % CI, 1.99-2.82, p = 0.033). The mutated HindIII genotype was significantly associated with increased TG and ApoB/ApoA-I ratio and with decreased HDL-C. Haplotype analysis showed that OR of SCS associated with the CTGTAG haplotype was 2.12 (95 % CI 1.05-4.25, p = 0.032) and with CGGGAA was 0.71 (95 % CI 0.26-1.95, p = 0.022) compared to the CTGTAA. Significant difference in Gensini score was observed among HindIII genotype and haplotypes. A significant association between the mutated genotype of HindIII polymorphism and decreased HDL-C level and increased ApoB/ApoA-I ratio and TG level was showed. Our results suggest that HindIII and D9N polymorphisms and CTGTAG haplotype seem to be considered as marker of predisposition to coronary stenosis. In another hand, HindIII and haplotypes were related to stenosis severity.

Association of LPL gene variant and LDL, HDL, VLDL cholesterol and triglyceride levels with ischemic stroke and its subtypes

Lipoprotein lipase (LPL) plays an important role in lipid metabolism by hydrolyzing triglycerides in chylomicrons and very low density lipoproteins. An increasing number of studies have suggested an association of LPL gene variants with the risk of cardiovascular and cerebrovascular diseases. The aim of this study was to test whether HindIII polymorphism of LPL gene is associated with ischemic stroke and its subtypes as well as plasma lipid levels in a South Indian population from Andhra Pradesh. Five hundred and twenty five ischemic stroke patients and 500 controls were enrolled in this case–control study. The LPL HindIII polymorphism was determined by PCR-RFLP technique and the lipid levels were estimated using commercially available kits. We found significant difference in the genotypic distribution between patients and controls [for HindIII (+/+) vs. HindIII (−/−), χ2=4.916; p=0.02; Odds ratio=1.59 (95%CI; 1.054–2.413); HindIII (+/+) vs. HindIII (−/−) and HindIII (+/−), χ2=5.25; p=0.02; Odds ratio=1.24 (95%CI; 1.03–1.503)]. A stepwise multiple logistic regression analysis confirmedthese findings. The relationship between HindIII genotypes and plasma levels of HDL, LDL, VLDL and triglycerides was analyzed using ANOVA and further confirmed by Post-hoc analysis. The levels of triglycerides were found to be elevated in individuals bearing HindIII (+/+) genotype in comparison with HindIII (−/−) genotype. HDL levels were found to be significantly reduced and triglyceride levels significantly elevated in HindIII (+/+) genotype in comparison with HindIII (−/−). However, there was no difference in the levels of LDL and VLDL between the two genotypes. Examining the association of LPL gene HindIII polymorphism with stroke subtypes, we found significant association of HindIII polymorphism with Intracranial large artery atherosclerosis [Odds ratio=2.12 955CI (1.656–2.848); p=0.009]. Our results suggest that the HindIII polymorphism of LPL is significantly associated with ischemic stroke risk and elevated levels of plasma triglycerides and reduced HDL levels. Further, this polymorphism is significantly associated with intracranial large artery atherosclerosis which is the most frequent subtype in our region.

Association of the HindIII and S447X polymorphisms in LPL gene with hypertension and type 2 diabetes in Mexican families.

Lipoprotein lipase (LPL) is a key enzyme in lipid metabolismand is associatedwith obesity, dyslipidemias, hypertension (HTN) and type 2 diabetes mellitus (T2DM). LPL gene polymorphisms can be related with the development of cardiovascular risk factors. The present study was conducted to analyze the relationship of the HindIII and S447X polymorphisms in LPL gene with cardiovascular risk factors in Mexican families. The study population comprised ninety members of 30 Mexican families, in which an index case had obesity, were included in the study. We evaluated the body composition by bioelectrical impedance. Peripheral blood samples were collected to determine biochemical parameters. Screening for both polymorphisms was made by PCR-RFLPs. In the parents, both polymorphisms were in Hardy-Weinberg’s equilibrium. We found that the genotype T/T of HindIII was associated with diastolic blood pressure ≧ 85 mmHg (OR = 1.1; p = 0.011), whereas the genotype C/C of S447X was associated with systolic blood pressure ≧ 130 mmHg (OR = 1.2; p < 0.001), diastolic blood pressure ≧ 85 mmHg (OR = 1.3; p < 0.001), T2DM (OR = 1.3; p < 0.001) and with increase of total cholesterol (β = 23.6 mg/mL; p = 0.03). These data suggest that the HindIII and S447X LPL gene polymorphisms can confer susceptibility for the development of hypertension and T2DM in Mexican families.

A novel single nucleotide polymorphism in exon 7 of LPL gene and its association with carcass traits and visceral fat deposition in yak (Bos grunniens) steers

Lipoprotein lipase (LPL) is considered as a key enzyme in the lipid deposition and metabolism in tissues. It is assumed to be a major candidate gene for genetic markers in lipid deposition. Therefore, the polymorphisms of the LPL gene and associations with carcass traits and viscera fat content were examined in 398 individuals from five yak (Bos grunniens) breeds using PCR-SSCP analysis and DNA sequencing. A novel nucleotide polymorphism (SNP)-C→T (nt19913) was identified located in exon 7 in the coding region of the LPL gene, which replacement was responsible for a Phe-to-Ser substitution at amino acid. Two alleles (A and B) and three genotypes designed as AA, AB and BB were detected in the PCR products. The frequencies of allele A were 0.7928, 0.7421, 0.7357, 0.6900 and 0.7083 for Tianzhu white yak (WY), Gannan yak (GY), Qinghai-Plateau yak (PY), Xinjiang yak (XY) and Datong yak (DY), respectively. The SNP loci was in Hardy-Weinberg equilibrium in five yak populations (P>0.05). Polymorphism of LPL gene was shown to be associated with carcass traits and lipid deposition. Least squares analysis revealed that there was a significant effect on live-weight (LW) (P<0.01), average daily weight gain (ADG) and carcass weight (P<0.05). Individuals with genotype BB had lower mean values than those with genotype AA and AB for loin eye area and viscera fat weight (% of LW) in 25-36 months (P<0.05). The results indicated that LPL gene is a strong candidate gene that affects carcass traits and fat deposition in yak.