血管紧张素转换酶插入/缺失（ACE I/D）和血管紧张素原（AGT M235T）多态性与突尼斯人群肥胖风险的关联。
Association of angiotensin-converting enzyme insertion/deletion (ACE I/D) and angiotensinogen (AGT M235T) polymorphisms with the risk of obesity in a Tunisian population.
机构信息
Biochemistry Laboratory, LR12ES05 "Nutrition-Functional Foods and Vascular Health", Faculty of Medicine, University of Monastir, Tunisia.
Department of Internal Medicine, CHU F. Bourguiba, Tunisia.
出版信息
J Renin Angiotensin Aldosterone Syst. 2020 Apr-Jun;21(2):1470320320907820. doi: 10.1177/1470320320907820.
Abstract
OBJECTIVE
This study aims to determine whether genetic variants in ACE I/D and AGT M235T are associated with overweight-obesity and body mass index (BMI) in a Tunisian population.
METHODS
We designed an age- and sex-matched case-control study. The height and weight were measured and BMI was calculated. A total of 259 overweight-obese patients and 369 healthy controls were genotyped for the ACE I/D and AGT M235T genes using polymerase chain reaction and restriction fragment length polymorphism.
RESULTS
ACE I/D and AGT M235T genes were associated with BMI, waist circumference and overweight-obesity (p⩽0.001). In an additive model, the I and the M alleles in ACE and AGT variants, respectively, were associated with a lower BMI: -1.45 and -2.29 units, respectively. ACE I/D genotypes were associated with dyslipidemia; AGT M235T genotypes with dyslipidemia and total cholesterol.
CONCLUSION
These data suggest that variations in ACE I/D and AGT M235T affect the risk of overweight-obesity, BMI and dyslipidemia, and could point to a key molecular pathway of metabolic syndrome and its related comorbidities.
摘要
目的
本研究旨在探讨 ACE I/D 和 AGT M235T 基因多态性与超重肥胖及体重指数（BMI）在突尼斯人群中的相关性。
方法
我们设计了一项年龄和性别匹配的病例对照研究。测量身高和体重，并计算 BMI。共对 259 名超重肥胖患者和 369 名健康对照者进行 ACE I/D 和 AGT M235T 基因的聚合酶链反应和限制性片段长度多态性检测。
结果
ACE I/D 和 AGT M235T 基因与 BMI、腰围和超重肥胖相关（p ⩽ 0.001）。在加性模型中，ACE 和 AGT 变异体中的 I 和 M 等位基因分别与较低的 BMI 相关：分别为-1.45 和-2.29 个单位。ACE I/D 基因型与血脂异常相关；AGT M235T 基因型与血脂异常和总胆固醇相关。
结论
这些数据表明，ACE I/D 和 AGT M235T 的变异影响超重肥胖、BMI 和血脂异常的风险，可能指出代谢综合征及其相关并发症的关键分子途径。
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