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Objective: 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[middle dot]2 /- 11[middle dot]3 years, body mass index (BMI) 24[middle dot]1 /- 3[middle dot]9) whose overnight fasting sera were available. Serum resistin was measured using ELISA.

Results: Serum resistin was higher in subjects with either obesity (P = 0[middle dot]041), low HDL (P = 0[middle dot]004), high triglycerides (TG) (P = 0[middle dot]019), hypertension (HT) (P = 0[middle dot]001) or atherosclerosis (P = 0[middle dot]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[middle dot]008), TG (P = 0[middle dot]041), HT (P = 0[middle dot]031) and hsCRP (P = 0[middle dot]004). Serum resistin was positively correlated with the number of MetS factors, independent of age, gender and the duration of T2DM (P < 0[middle dot]001). Adjustment by either thiazolidinedione (TZD) treatment or hsCRP had no effects on these findings.

Conclusions: Serum resistin was positively correlated with the accumulation of MetS factors in T2DM.

Copyright (C) 2008 Blackwell Publishing Ltd.