LEP -2548G>A Polymorphism of the Leptin Gene and Its Influence on the Lipid Profile in Obese Individuals.

Q Agricultural and Biological Sciences

Journal of Nutrigenetics and Nutrigenomics Pub Date : 2014-01-01 Epub Date: 2015-03-17 DOI:10.1159/000371767

Maysa Araujo Ferreira-Julio, Marcela Souza Pinhel, Driele Cristina Gomes Quinhoneiro, Carolina Ferreira Nicoletti, Antonio Carlos Brandão, Carla Barbosa Nonino, Sidney Pinheiro, Bruno Affonso Parenti Oliveira, Michele Lima Gregório, Days Oliveira Andrade, Cristiana Cortes-Oliveira, Dorotéia Silva Souza

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引用次数: 5

Abstract

Background/aim: We studied the molecular pathogenesis of obesity, involving complex interactions between environmental and genetic factors, with a focus on the leptin gene. It was our aim to characterize the LEP -2548G>A leptin polymorphism and lipid profile in obese and normal-weight individuals.

Methods: A total of 212 individuals were divided into the study group including 136 obese patients (body mass index, BMI≥30) and the control group with 76 normal-weight individuals (BMI>18.5 and ≤24.9). DNA was amplified by polymerase chain reaction and restriction fragment length polymorphism. The lipid profile was analyzed by enzymatic colorimetric methods. The level of significance was set at p<0.05.

Results: There was a prevalence of the GA genotype in both groups. However, comparative group analysis showed an association of the recessive model (AA+GA) with increased triglycerides (TG) and decreased high-density lipoprotein cholesterol (HDL-C) levels in the study group.

Conclusion: This study did not confirm an association between obesity and the LEP -2548G>A polymorphism. However, AA+GA genotypes, in the presence of obesity, seem to contribute to a reduction in HDL-C and an increase in TG compared with normal-weight individuals. This should be confirmed in further studies.

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肥胖人群瘦素基因LEP -2548G>A多态性及其对血脂的影响

背景/目的:我们研究了肥胖的分子发病机制，涉及环境和遗传因素之间的复杂相互作用，重点研究了瘦素基因。我们的目的是表征肥胖和正常体重个体的LEP -2548G>A瘦素多态性和脂质谱。方法:将212例患者分为研究组136例肥胖患者(体重指数，BMI≥30)和对照组76例体重正常患者(BMI>18.5≤24.9)。采用聚合酶链反应和限制性片段长度多态性扩增DNA。用酶比色法分析脂质谱。显著性水平设为结果:两组均存在GA基因型的患病率。然而，对照组分析显示，在研究组中，隐性模型(AA+GA)与甘油三酯(TG)升高和高密度脂蛋白胆固醇(HDL-C)降低存在关联。结论:本研究未证实肥胖与LEP -2548G>A多态性之间存在关联。然而，与体重正常的人相比，AA+GA基因型，在肥胖的情况下，似乎有助于降低HDL-C和增加TG。这应该在进一步的研究中得到证实。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Journal of Nutrigenetics and Nutrigenomics GENETICS & HEREDITY-NUTRITION & DIETETICS

CiteScore

1.86

自引率

0.00%

发文量

审稿时长

>12 weeks

期刊介绍： The emerging field of nutrigenetics and nutrigenomics is rapidly gaining importance, and this new international journal has been established to meet the needs of the investigators for a high-quality platform for their research. Endorsed by the recently founded "International Society of Nutrigenetics/Nutrigenomics", the ‘Journal of Nutrigenetics and Nutrigenomics’ welcomes contributions not only investigating the role of genetic variation in response to diet and that of nutrients in the regulation of gene expression, but is also open for articles covering all aspects of gene-environment interactions in the determination of health and disease.