Apolipoprotein A5-12238 T&gt;C gene polymorphism and risk factors for metabolic syndrome in the Guo Shan Yao and the Han populations

He, Fuchu; Xu, Xin; Hu, Deming; S.K., Edmond; Tang, Lina; Fan, Wenmao; Chen, Baofeng; Zhang, Jianying; Ma, Zhu

doi:10.1515/cclm.2011.243

Cited by 2 publications

(7 citation statements)

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“…Grallert et al (2007) systematically analyzed 10 APOA5 gene polymorphisms for association with metabolic syndrome in two relatively large studies in southern Germany (KORA, N = 1354) and in Austria (SAPHIR, N = 1770). Also, the variant alleles of IVS3 + 476G>A and −12238T>C polymorphisms of APOA5 have been reported to represent risk factors for this condition (Kisfali et al, 2008;He et al, 2011). These results were subsequently confirmed by Dallongeville et al (2008) who reported that variant c.56C>G increased susceptibility to metabolic syndrome in subjects from France.…”

Section: (2) Apoa5 Snps and Association With The Metabolic Syndromementioning

confidence: 74%

“…Biological Reviews © 2012 Cambridge Philosophical Society genes in almost 2500 subjects and controls and demonstrated that minor alleles at 2 of the APOA5 SNPs examined (c.−3A>G and c.553G>T) were significantly associated with increased metabolic syndrome risk (Yamada et al, 2008b). Also, the variant alleles of IVS3 + 476G>A and −12238T>C polymorphisms of APOA5 have been reported to represent risk factors for this condition (Kisfali et al, 2008;He et al, 2011).…”

Section: (2) Apoa5 Snps and Association With The Metabolic Syndromementioning

confidence: 99%

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The role of apolipoprotein A5 in obesity and the metabolic syndrome

2012

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Apolipoprotein A5 (apoA5) has an important role in lipid metabolism, specifically for triglyceride-rich lipoproteins. Recently, evidence has emerged for an association between genetic variability at the APOA5 locus and increased risk of obesity and metabolic syndrome. However, its mechanism of action remains to be fully elucidated. Importantly, an intracellular role of apoA5 has been indicated since apoA5 is associated with cytoplasmic lipid droplets and affects intrahepatic triglyceride accumulation, as well as affecting intravascular triglyceride metabolism. Given that adipocytes provide the largest storage depot for energy in the form of triglyceride within the lipid droplets, and play a crucial role in the development of obesity, we highlight recent findings discussing the interaction of apoA5 with adipocytes or adipose tissue, indicating that apoA5 may act as a novel regulator to modulate triglyceride storage in adipocytes. We review the association of APOA5 gene polymorphisms with obesity and metabolic syndrome, and propose potential mechanisms by which apoA5 may increase susceptibility to these conditions. This review provides new insights into the physiological role of apoA5 and identifies a potential therapeutic target for obesity and associated disorders.

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Section: (2) Apoa5 Snps and Association With The Metabolic Syndromementioning

confidence: 74%

Section: (2) Apoa5 Snps and Association With The Metabolic Syndromementioning

confidence: 99%

The role of apolipoprotein A5 in obesity and the metabolic syndrome

2012

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“…All studies have cross-sectional design. Most studies were from Asia ( n = 17) [ 11 , 15 , 22 , 24 , 26 , 29 – 32 , 34 – 36 , 48 , 49 , 52 , 55 , 57 ] and Europe ( n = 8) [ 27 , 33 , 46 , 47 , 50 , 51 , 54 , 56 ], while we found just one study that was conducted in the USA [ 53 ], and four studies that were from Africa [ 19 , 21 , 25 , 28 ]. The age range of the participants was 18 to 79, and the majority of studies were performed among both sexes, while three studies included only women [ 31 , 32 , 51 ].…”

Section: Resultsmentioning

confidence: 99%

“…The age range of the participants was 18 to 79, and the majority of studies were performed among both sexes, while three studies included only women [ 31 , 32 , 51 ]. Twenty-two studies were consistent with Hardy-Weinberg equilibrium (HWE) [ 11 , 21 , 22 , 24 , 25 , 27 , 29 , 30 , 32 – 35 , 46 , 48 – 51 , 53 – 57 ]. However, in three studies, HWE was not in equilibrium [ 15 , 36 , 47 ], and in six studies, HWE was not reported [ 19 , 24 , 26 , 28 , 31 , 52 ].…”

Section: Resultsmentioning

confidence: 99%

“…However, in three studies, HWE was not in equilibrium [ 15 , 36 , 47 ], and in six studies, HWE was not reported [ 19 , 24 , 26 , 28 , 31 , 52 ]. Seventeen studies used NCEP ATP III criteria [ 11 , 22 , 27 , 28 , 31 – 34 , 46 , 47 , 49 – 54 , 56 ], ten studies used IDF criteria [ 15 , 19 , 21 , 24 , 25 , 29 , 30 , 35 , 36 , 48 ], and three studies used modified definition for identifying MetS [ 26 , 55 , 57 ]. Several techniques were used to identify the genotypes, such as the Polymerase Chain Reaction -Amplification Refractory Mutation System (PCR-RFLP) [ 15 , 19 , 22 , 28 , 31 , 46 , 48 – 50 , 54 , 56 ], Real-Time PCR Taqman [ 27 , 33 , 34 , 51 , 53 ], PCR and sequence-specific oligonucleotide probes (PCR-SSOP) [ 11 , 30 , 57 ], Mass Array [ 29 , 52 , 55 ], Matrix-Assisted Laser Desorption/Ionization (MALDI-TOF) [ 35 , 47 ], Kaspar technology [ 21 , 25 ], SNP Integration Tool (SNP-IT) assay [ 32 ], and bead-based microarray tech [ 24 ,…”

Section: Resultsmentioning

confidence: 99%

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Association between APOA5 polymorphisms and susceptibility to metabolic syndrome: a systematic review and meta-analysis

Mozafari,

Ashoori,

Emami Meybodi

et al. 2024

BMC Genomics

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Background The association between Apolipoprotein A5 (APOA5) genetic polymorphisms and susceptibility to metabolic syndrome (MetS) has been established by many studies, but there have been conflicting results from the literature. We performed a meta-analysis of observational studies to evaluate the association between APOA5 gene polymorphisms and the prevalence of MetS. Methods PubMed, Web of Science, Embase, and Scopus were searched up to April 2024. The random effects model was used to estimate the odds ratios (ORs) and 95% confidence intervals (CI) of the association between APOA5 gene polymorphisms and the prevalence of MetS development. The potential sources of heterogeneity were evaluated by subgroup analyses and sensitivity analyses. Results A total of 30 studies with 54,986 subjects (25,341 MetS cases and 29,645 healthy controls) were included. The presence of rs662799 and rs651821 polymorphisms is associated with an approximately 1.5-fold higher likelihood of MetS prevalence (OR = 1.42, 95% CI: 1.32, 1.53, p < 0.001; I2 = 67.1%; P-heterogeneity < 0.001; and OR = 1.50, 95% CI: 1.36–1.65, p < 0.001), respectively. MetS is also more prevalent in individuals with the genetic variants rs3135506 and rs2075291. There was no evidence of a connection with rs126317. Conclusion The present findings suggest that polymorphisms located in the promoter and coding regions of the APOA5 gene are associated with an increased prevalence of MetS in the adult population. Identifying individuals with these genetic variations could lead to early disease detection and the implementation of preventive strategies to reduce the risk of MetS and its related health issues. However, because the sample size was small and there was evidence of significant heterogeneity for some APOA5 gene polymorphisms, these results need to be confirmed by more large-scale and well-designed studies.

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Apolipoprotein A5-12238 T>C gene polymorphism and risk factors for metabolic syndrome in the Guo Shan Yao and the Han populations

Cited by 2 publications

References 10 publications

The role of apolipoprotein A5 in obesity and the metabolic syndrome

The role of apolipoprotein A5 in obesity and the metabolic syndrome

Association between APOA5 polymorphisms and susceptibility to metabolic syndrome: a systematic review and meta-analysis

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