InsulIn resIstance (Ir) is characterized by a decreased capacity of insulin to perform its normal physiological functions. IR is regulated by both environmental and genetic factors [1,2], and is considered as the core factor in the pathogenesis of metabolic syndrome and obesity. In recent years, numerous studies have revealed abundant information about the molecular mechanism of IR [3,4]. However, the exact pathogenesis underlying the development and progression of IR remains unclear.Adiponectin, the most abundant adipocyte-derived protein, is involved in the control of glucose, fat metabolism, and insulin sensitivity [5,6]. Adiponectindeficient mice exhibit IR and glucose intolerance [7,8], and animal models of obesity and IR show reduced plasma adiponectin levels [9,10]. Adiponectin exerts a potent insulin-sensitizing effect through its receptors AdipoR1 and AdipoR2, leading to the activation Association of the ADIPOQ T45G polymorphism with insulin resistance and blood glucose: A meta-analysis Results of published studies on the association of the ADIPOQ T45G polymorphism with insulin resistance (IR) and blood glucose are conflicting. In this study, we performed a meta-analysis to further investigate such an association. Articles that evaluate the effect of the T45G polymorphism on IR and blood glucose were identified from the PubMed and Embase databases. Five indices, including fasting blood glucose (FBG), fasting insulin (F-insulin), 2-h blood glucose (2-h BG), 2-h insulin, and homeostasis model assessment insulin resistance index (HOMA-IR), were used to assess the effects of the T45G polymorphism on IR and blood glucose under a dominant model. 24 articles involving 7630 subjects were included. Twenty-two studies on FBG, 17 on F-insulin, 20 on HOMA-IR, and 3 on 2-h BG were included. No study on 2-h insulin was found. This meta-analysis revealed no significant association between the ADIPOQ T45G polymorphism and IR and blood glucose in the overall population and subgroup subjects under a dominant model, regardless of whether FBG, F-insulin, 2-h BG, or HOMA-IR was used. The present meta-analysis indicated that the mutation allele may have no function in IR development. The ADIPOQ T45G polymorphism is not associated with IR and blood glucose.