Endocrinology and Nutrition Service, Hospital Carlos Haya, Malaga, Spain.
J Rheumatol. 2010 Feb;37(2):417-21. doi: 10.3899/jrheum.090637. Epub 2009 Dec 15.
To study the role of Trp64Arg polymorphism of the ADRB3 gene in the risk of developing hyperuricemia in 1051 subjects from southern Spain, with a followup of 6 years. The inclusion of plasma levels of uric acid as a diagnostic criterion to define the metabolic syndrome is under discussion. Genes responsible for insulin resistance could contribute to the development of hyperuricemia. Previous cross-sectional studies have suggested ADRB3 as a possible candidate gene in the development of hyperuricemia and insulin resistance.
A prospective, population-based, cohort study of 1051 persons examined in 1997-98 and reassessed at a second examination 6 years later. The metabolic phenotype was assessed at baseline and again at the followup. Insulin resistance was measured by homeostasis model assessment. The Trp64Arg polymorphism of ADRB3 was detected by real-time polymerase chain reaction. Subjects were considered normouricemic if their serum uric acid levels were <or=7 mg/dl for men or <or= 6 mg/dl for women.
Carriers of the Arg64 allele who were normouricemic at baseline had a higher risk of developing hyperuricemia 6 years later (p = 0.017, OR 2.3, 95% CI 1.1-4.6). Multivariate logistic regression analysis showed that the OR of having hyperuricemia at the 6-year followup was significantly associated with the Arg64 allele, after adjusting for age, weight gain, baseline levels of triglycerides, serum uric acid, and insulin resistance (OR 3.1, 95% CI 1.3-7.1).
Trp64Arg polymorphism of the ADRB3 gene predicted the risk of developing hyperuricemia in this adult population.
在西班牙南部的 1051 名受试者中，研究 ADRB3 基因的 Trp64Arg 多态性在 6 年随访期间发生高尿酸血症的风险。目前正在讨论将血浆尿酸水平作为诊断标准纳入代谢综合征的定义。胰岛素抵抗相关基因可能导致高尿酸血症的发生。先前的横断面研究表明 ADRB3 可能是高尿酸血症和胰岛素抵抗发展的候选基因。
这是一项前瞻性、基于人群的队列研究，共纳入 1051 名受试者，于 1997-98 年进行初次检查，并在 6 年后的第二次检查中进行了重新评估。在基线和随访时评估代谢表型。通过稳态模型评估胰岛素抵抗。使用实时聚合酶链反应检测 ADRB3 的 Trp64Arg 多态性。如果男性血清尿酸水平<或=7mg/dl，女性<或=6mg/dl，则受试者被认为血尿酸正常。
在基线时血尿酸正常且携带 Arg64 等位基因的受试者，6 年后发生高尿酸血症的风险更高（p=0.017，OR 2.3，95%CI 1.1-4.6）。多变量逻辑回归分析显示，在校正年龄、体重增加、基线甘油三酯、血清尿酸和胰岛素抵抗后，Arg64 等位基因与 6 年随访时发生高尿酸血症的 OR 显著相关（OR 3.1，95%CI 1.3-7.1）。
ADRB3 基因的 Trp64Arg 多态性预测了该成年人群发生高尿酸血症的风险。
