Osawa Haruhiko, Ochi Masaaki, Tabara Yasuharu, Kato Kenichi, Yamauchi Junko, Takata Yasunori, Nishida Wataru, Onuma Hiroshi, Shimizu Ikki, Fujii Yasuhisa, Miki Tetsuro, Ohashi Jun, Makino Hideichi
Department of Molecular and Genetic Medicine, Ehime University Graduate School of Medicine, Ehime Prefectural Hospital, Ehime, Japan.
Clin Endocrinol (Oxf). 2008 Jul;69(1):74-80. doi: 10.1111/j.1365-2265.2007.03154.x. Epub 2008 Jul 1.
Resistin, secreted from adipocytes, causes insulin resistance in rodents. We reported that the G/G genotype of a resistin gene promoter single nucleotide polymorphism (SNP) at -420 increases type 2 diabetes (T2DM) susceptibility by enhancing promoter activity. We also showed that serum resistin was positively correlated with G at SNP-420, the duration of T2DM, and HbA1c in T2DM. The aim of this study was to determine the relation between serum resistin and factors related to the metabolic syndrome (MetS) in T2DM.
DESIGN, PATIENTS AND MEASUREMENTS: We analysed 238 Japanese T2DM subjects (124 males and 114 females, age 60.2 +/- 11.3 years, body mass index (BMI) 24.1 +/- 3.9) whose overnight fasting sera were available. Serum resistin was measured using ELISA.
Serum resistin was higher in subjects with either obesity (P = 0.041), low HDL (P = 0.004), high triglycerides (TG) (P = 0.019), hypertension (HT) (P = 0.001) or atherosclerosis (P = 0.012). Simple regression analysis revealed that serum resistin was correlated with lower HDL, TG and high-sensitivity C-reactive protein (hsCRP). Multiple regression analysis (or logistic regression analysis for HT), adjusted for age, gender, BMI and the duration of T2DM, revealed that serum resistin was correlated with lower HDL (P = 0.008), TG (P = 0.041), HT (P = 0.031) and hsCRP (P = 0.004). Serum resistin was positively correlated with the number of MetS factors, independent of age, gender and the duration of T2DM (P < 0.001). Adjustment by either thiazolidinedione (TZD) treatment or hsCRP had no effects on these findings.
Serum resistin was positively correlated with the accumulation of MetS factors in T2DM.
脂肪细胞分泌的抵抗素可导致啮齿动物出现胰岛素抵抗。我们曾报道,抵抗素基因启动子位于-420处的单核苷酸多态性(SNP)的G/G基因型可通过增强启动子活性增加2型糖尿病(T2DM)易感性。我们还表明,血清抵抗素与SNP-420处的G、T2DM病程以及T2DM患者的糖化血红蛋白(HbA1c)呈正相关。本研究旨在确定T2DM患者血清抵抗素与代谢综合征(MetS)相关因素之间的关系。
设计、患者与测量:我们分析了238例日本T2DM患者(男性124例,女性114例,年龄60.2±11.3岁,体重指数(BMI)24.1±3.9),这些患者均有过夜空腹血清。采用酶联免疫吸附测定法(ELISA)检测血清抵抗素。
肥胖(P = 0.041)、高密度脂蛋白(HDL)低(P = 0.004)、甘油三酯(TG)高(P = 0.019)、高血压(HT)(P = 0.001)或动脉粥样硬化(P = 0.012)患者的血清抵抗素水平较高。简单回归分析显示,血清抵抗素与较低的HDL、TG和高敏C反应蛋白(hsCRP)相关。在对年龄、性别、BMI和T2DM病程进行校正后的多元回归分析(或针对HT的逻辑回归分析)显示,血清抵抗素与较低的HDL(P = 0.008)、TG(P = 0.041)、HT(P = 0.031)和hsCRP(P = 0.004)相关。血清抵抗素与MetS因素数量呈正相关,不受年龄、性别和T2DM病程影响(P < 0.001)。噻唑烷二酮(TZD)治疗或hsCRP校正对这些结果无影响。
T2DM患者血清抵抗素与MetS因素的聚集呈正相关。