Institute of Endocrinology and Nutrition, Medicine School and Unit of Investigation, Hospital Rio Hortega, University of Valladolid, RD056/00013 RETICEF, Valladolid, Spain.
Obes Surg. 2009 Dec;19(12):1691-6. doi: 10.1007/s11695-009-9859-x.
A transition G to A at codon 54 of fatty acid binding protein 2 (FABP2) results in an amino acid substitution (ala 54 to Thr 54). This polymorphism was associated with insulin resistance in some populations.
The aim of our study was to investigate the influence of Thr54 polymorphism in the FABP2 gene on obesity anthropometric parameters, cardiovascular risk factors, and adipocytokines in patients with presurgical morbid obesity.
A population of 55 morbid obese patients was enrolled. An indirect calorimetry, tetrapolar electrical bioimpedance, blood pressure, a serial assessment of nutritional intake with 3 days of written food records, and biochemical analysis (lipid profile, adipocytokines, insulin, C-reactive protein, and lipoprotein-a) were performed. The statistical analysis was performed for the combined Ala54/Thr54 and Thr54/Thr54 as a mutant-type group and wild-type group (Ala54/Ala54).
Twenty nine (52.7%) had the genotype Ala54/Ala54 (wild-type group) and 26 (47.3%) patients had the genotype Ala54/Thr54 (24 patients, 43.7%) or Thr54/Thr54 (two patients, 3.6%; mutant-type group). Insulin (22.4 +/- 16.8 vs. 26.1 +/- 17.1 mg/dl; p = 0.04) and homeostasis model assessment (6.1 +/- 2.1 vs. 6.7 +/- 4.5; p = 0.04) levels were higher in mutant-type group than wild-type group. In mutant-type group, leptin levels (134.8 +/- 83 vs. 206.5 +/- 76 ng/ml; p = 0.03) were higher than wild-type group. Moreover, adiponectin levels (80.9 +/- 39.6 vs. 23.9 +/- 13.8 ng/ml; p = 0.02) were higher in wild-type group than mutant-type group.
The novel finding of this study is the association of Thr54 allele with insulin resistance, leptin, and adiponectin levels in morbidly obese patients.
脂肪酸结合蛋白 2(FABP2)密码子 54 处的 G 到 A 转换导致氨基酸取代(丙氨酸 54 突变为苏氨酸 54)。这种多态性与一些人群的胰岛素抵抗有关。
我们研究的目的是探讨 FABP2 基因中 Thr54 多态性对术前病态肥胖患者肥胖人体测量参数、心血管危险因素和脂肪细胞因子的影响。
纳入了 55 名病态肥胖患者。进行了间接热量测定、四极电生物阻抗、血压、连续 3 天书面食物记录的营养摄入量评估以及生化分析(血脂谱、脂肪细胞因子、胰岛素、C 反应蛋白和脂蛋白-a)。统计分析针对 Ala54/Thr54 和 Thr54/Thr54 联合作为突变型组和野生型组(Ala54/Ala54)进行。
29 名(52.7%)患者携带 Ala54/Ala54 基因型(野生型组),26 名(47.3%)患者携带 Ala54/Thr54 基因型(24 名,43.7%)或 Thr54/Thr54 基因型(2 名,3.6%;突变型组)。突变型组胰岛素(22.4±16.8 与 26.1±17.1mg/dl;p=0.04)和稳态模型评估(6.1±2.1 与 6.7±4.5;p=0.04)水平高于野生型组。在突变型组中,瘦素水平(134.8±83 与 206.5±76ng/ml;p=0.03)高于野生型组。此外,野生型组的脂联素水平(80.9±39.6 与 23.9±13.8ng/ml;p=0.02)高于突变型组。
本研究的新发现是 Thr54 等位基因与病态肥胖患者的胰岛素抵抗、瘦素和脂联素水平相关。