肥胖儿童及青少年瘦素、脂联素及脂联素基因多态性及瘦素受体分析

Daniela Šupe Domić, Ivana Unić Šabašov, Lada Stanišić, Sunčana Janković, Milena Nadrčić, A. Matana, E. Čečuk-Jeličić, I. Drmić Hofman
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引用次数: 0

摘要

背景:本研究旨在测定肥胖儿童血清瘦素和脂联素水平,探讨瘦素受体基因多态性对瘦素抵抗和瘦素水平的影响,以及脂联素基因多态性与脂联素水平的关系。材料与方法:采用病例对照研究,将74例肥胖儿童(年龄13.34±2.60岁)与69例体重年龄正常(年龄13.39±2.64岁)对照组进行比较。两组均测量了身体质量指数(BMI)、腰围/臀围、收缩压和舒张压。同时测定瘦素和脂联素水平、糖脂代谢参数、高敏感c反应蛋白(hs-CRP)。采用空腹胰岛素血症和胰岛素抵抗稳态模型评估(HOMA-IR)评估胰岛素敏感性。对所有受试者进行LEPRQ223R (rs1137101)、ADIPOQ G276T (rs1501299)和ADIPOT45G (rs2241766)基因多态性检测。结果:肥胖儿童研究组在体重、BMI、腰臀围、收缩压等表型上均显著高于对照组(P<0.001)。我们证实,肥胖儿童血液中瘦素水平升高,脂联素水平降低(P<0.001)。肥胖儿童研究组与对照组瘦素受体(LEPRQ223R)和脂联素(ADIPOG276T和ADIPOT45G)基因多态性的基因型分布差异不观察。结论:在本研究中,我们发现肥胖儿童组与对照组相比,瘦素水平升高,脂联素水平显著降低。两组间糖代谢及血脂分析结果显示,与对照组相比,肥胖儿童组胰岛素、HOMA-IR、甘油三酯、hsCRP均升高,且差异显著,如预期。然而,通过包括大量的性别和年龄特定群体的测试和对照样本,以及大量测试的SNPs,本研究中调查的基因可能会更好地了解诸如肥胖之类的多复杂疾病。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Analysis of leptin, adiponectin and adiponectin gene polymorphism and leptin receptor in obese children and adolescents
Background: The aim of this study was to determine serum levels of leptin and adiponectin of obese children to identify the influence of leptin receptor gene polymorphisms on leptin resistance and leptin levels, as well as the association between the polymorphisms of adiponectin gene and adiponectin levels.Materials and methods: A case-control study comparing a study group of 74 obese children (age 13.34±2.60 years) to a normal weight-age matched (age 13.39±2.64 years) control group of 69 children. In both groups, body mass index (BMI) and waist/hip circumference, systolic and diastolic blood pressure were measured. Also, the leptin and adiponectin levels, as well as glucose and lipid metabolism parameters, and highly sensitive C-reactive protein (hs-CRP) were measured. Insulin sensitivity was evaluated using fasting insulinemia and Homeostatic Model Assessment for Insulin Resistance (HOMA-IR). All subjects were tested for gene-tic polymorphisms in LEPRQ223R (rs1137101), ADIPOQ G276T (rs1501299) and ADIPOT45G (rs2241766).Results: The phenotypes of the obese children study group were significantly higher than in the control group in weight, BMI, waist/hip circumferences and systolic blood pressure (SBP) (P<0.001). We confirmed that in obese children the levels of leptin in the blood are increased and levels of adiponectin are decreased (P<0.001). The differences of the genotype distributions of leptin receptor (LEPRQ223R) and adiponectin (ADIPOG276T and ADIPOT45G) gene polymorphisms in the study group of obese chil-dren and a control group was not observed.Conclusion: In this study, we demonstrated increased leptin level and significantly decreased level of adiponectin in the obese children group compared with the control group. The results of the analysis of glucose metabolism and lipidogram between the two groups showed that insulin, HOMA-IR, and triglycerides, as well as hsCRP were increased and significantly different in the group of obese children compared to the control group, as expected. However, by including a significantly larger number of tested and control samples of both sexes and age-specific groups, with a larger number of tested SNPs, the genes investigated in this study would probably give better insight into a multicomplex disease such as obesity.
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