期刊
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
卷 93, 期 2, 页码 578-583出版社
ENDOCRINE SOC
DOI: 10.1210/jc.2007-2185
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资金
- NCCIH NIH HHS [K24 AT 00596, K24 AT000596] Funding Source: Medline
- NIDDK NIH HHS [R21 DK069801, DK69801, R33 DK069801] Funding Source: Medline
Context: Type 1 diabetes (T1DM) is associated with increased cardiovascular mortality. It is a proinflammatory state as evidenced by increased circulating biomarkers and monocyte activity. The toll-like receptors (TLRs) are pattern recognition receptors, expressed abundantly on monocytes. TLR2 and TLR4 are important in atherosclerosis. However, there is a paucity of data examining TLR2 and TLR4 expression in T1DM and examining its contribution to the proinflammatory state. Objective: Thus, we examined TLR2 and TLR4 expression in monocytes from T1DM patients compared with controls (n = 31 per group). Setting: The study was performed at the University of California Davis Medical Center. Patients: Healthy controls (n = 31) and T1DM patients (n = 31) were included in the study. Results: TLR2 and TLR4 surface expression and mRNA were significantly increased in T1 DIM monocytes compared with controls. Downstream targets of TLR, nuclear factor kappa B, myeloid differentiation factor 88, Trif, and phosphorylated IL-1 receptor-associated kinase were significantly up-regulated in T1DM. Finally, the release of IL-1 beta and TNF-alpha was significantly increased in monocytes from T1DM compared with controls and correlated with TLR2 and TLR4 expression (P < 0.005). In addition, TLR2 and TLR4 expression was significantly correlated to glycosylated hemoglobin, carboxymethyllysine, and nuclear factor kappa B (P < 0.02). Conclusion: Thus, we make the novel observation that TLR2 and TLR4 expression and signaling are increased in T1DM and contribute to the proinflammatory state.
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