Suppr超能文献

体重增加易感性的群体遗传学分析。

Population genetic analyses of susceptibility to increased body weight.

机构信息

Physical Medicine and Rehabilitation Department, University Children's Hospital, Belgrade, Serbia.

出版信息

Arch Med Sci. 2012 Dec 20;8(6):998-1002. doi: 10.5114/aoms.2012.32405. Epub 2012 Dec 19.

Abstract

INTRODUCTION

Obesity is a complex condition with multifactorial origin. Assuming that such a state is genetically controlled, the aim of our study was to evaluate the degree of genetic homozygosity among overweight and obese individuals by the homozygously recessive characteristics (HRC) test.

MATERIAL AND METHODS

We analysed the presence, distribution and individual combination of 15 selected genetically controlled recessive phenotype traits in a sample of 140 individuals with increased body mass index (overweight individuals n = 100 and obese individuals n = 40) and a control group of normal weight individuals (n = 300).

RESULTS

OBESE INDIVIDUALS HAVE SIGNIFICANTLY HIGHER MEAN VALUES FOR GENETIC HOMOZYGOSITY THAN THOSE WITH NORMAL WEIGHT (NORMAL WEIGHT: 3.61 ±1.48; obese: 4.13 ±1.47, p < 0.05) and difference in the presence of certain individual combinations of evaluated phenotype traits (Σχ(2) = 76.9; p < 0.01). There was no difference in average homozygosity of such genetic markers between groups of normal weight and overweight individuals (normal weight: 3.61 ±1.48; overweight: 3.93 ±1.51, p > 0.05) and between groups of overweight and obese individuals (overweight: 3.93 ±1.51; obese: 4.13 ±1.47, p > 0.05). There is no difference in the presence of certain individual combinations of evaluated phenotype traits between overweight and obese individuals (Σχ(2) = 20.6; p > 0.05).

CONCLUSIONS

There is a populational genetic difference in the degree of genetic homozygosity and variability between the group of normal weight and group of obese individuals, indicating a possible genetic component. Overweight and obese individuals have a genetic predisposition, but different expression of genetic loads could be one of the possible explanations for different susceptibility to increase of fat mass and body mass index.

摘要

引言

肥胖是一种具有多因素起源的复杂病症。假设这种状态是由基因控制的,我们的研究目的是通过纯合隐性特征(HRC)测试评估超重和肥胖个体的遗传同型程度。

材料与方法

我们分析了 140 名体重指数增加的个体(超重个体 n=100 例,肥胖个体 n=40 例)和正常体重个体对照组(n=300 例)样本中 15 种选定的遗传控制隐性表型特征的存在、分布和个体组合。

结果

肥胖个体的遗传同型性平均值明显高于体重正常个体(体重正常:3.61 ±1.48;肥胖:4.13 ±1.47,p<0.05),并且在评估表型特征的某些个体组合的存在方面存在差异(Σχ(2)=76.9;p<0.01)。体重正常和超重个体组之间以及超重和肥胖个体组之间,此类遗传标记的平均同型性没有差异(体重正常:3.61 ±1.48;超重:3.93 ±1.51,p>0.05)。超重和肥胖个体组之间,以及超重和肥胖个体组之间,评估表型特征的某些个体组合的存在也没有差异(Σχ(2)=20.6;p>0.05)。

结论

体重正常组和肥胖组之间遗传同型性和变异性程度存在群体遗传差异,表明可能存在遗传因素。超重和肥胖个体具有遗传易感性,但遗传负荷的不同表达可能是对脂肪量和体重指数增加的易感性不同的原因之一。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eeef/3542489/2204974e2c70/AMS-8-19911-g001.jpg

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验