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Low serum levels of the innate immune component ficolin-3 is associated with insulin resistance and predicts the development of type 2 diabetes Free
Haibing Chen, Junxi Lu, Xie Chen, Haoyong Yu, Lei Zhang, Yuqian Bao, Fengdi Lu, Junling Tang, Chenchen Gu, and Weiping Jia*
Shanghai Diabetes Institute, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Clinical Center for Diabetes, Department of Endocrinology and Metabolism, Shanghai Jiaotong University Affiliated Sixth People's Hospital, Shanghai 200233, China *Correspondence to:Weiping Jia, E-mail: wpjia@sjtu.edu.cn
J Mol Cell Biol, Volume 4, Issue 4, August 2012, 256-257,  https://doi.org/10.1093/jmcb/mjs032

Impaired insulin secretion and insulin resistance are the two main mechanisms that lead to type 2 diabetes mellitus (T2DM). Insulin resistance associated with innate immune system is known to be triggered by the activation of pattern-recognition receptors (PRRs) (Olefsky and Glass, 2010). Recently, our research group showed that serum ficolin-3, a kind of soluble PRR within the lectin pathway varied significantly between individuals with normal glucose tolerance (NGT) and those with T2DM (Li et al., 2008).
Here we performed a human cross-sectional study and a prospective study to investigate whether serum ficolin-3 levels associate with insulin resistance and predict the incidence of T2DM.
In the cross-sectional study, in which 170 had NGT and 95 had T2DM without any diabetic complications, we found that serum ficolin-3 in the T2DM group was significantly lower than that in the NGT group and multiple linear stepwise regression analyses revealed that serum ficolin-3 was independently correlated with high-density lipoprotein-cholesterol (HDL-c), homeostasis model assessment index of insulin resistance (HOMA-IR), hemoglobin A1c (HbA1c), and age (Supplementary Tables S1 and S2). The glucose disposal rate (GDR) used as a measurement of insulin sensitivity by euglycemic–hyperinsulinemic clamp technique was positively correlated with serum ficolin-3 in 51 NGT subjects (Figure 1A).