Increased Toll-Like Receptor 2 Expression in Peptidoglycan-Treated Blood Monocytes Is Associated with Insulin Resistance in Patients with Nondiabetic Rheumatoid Arthritis

Shih-Wei Wang,Chiou-Huey Wang,Hsiao-Han Liu,Tsun-Mei Lin,Jer-Yiing Houng

doi:10.1155/2012/690525

Shih-Wei Wang, Chiou-Huey Wang + Show 3 more

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https://doi.org/10.1155/2012/690525

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Abstract

The close relationship between increased TLR-2 expression in blood monocytes and insulin resistance in RA patients is shown in this study. Traditional risk factors for metabolic disorders, including the waist circumstance, body mass index (BMI), triglyceride (TG), and ratio of TG to high density lipoprotein (HDL) cholesterol, were closely correlated with HOMA (homoeostasis model assessment) index in patients with nondiabetic RA. Expressions of TLR2 in peripheral blood monocytes, following stimulation with peptidoglycan which is known as a TLR2 agonist, were closely correlated with the HOMA index, TNF-α, and IL-6 concentrations. Accordingly, TLR-2 receptor and its related inflammatory cytokines could be potential therapeutic targets in managing insulin resistance in RA patients.

Highlights

Rheumatoid arthritis (RA) is a complex disease whose pathogenesis remains unknown
The present study found that TLR2 expression in circulating CD14+ monocytes, after stimulation with peptidoglycan, correlated significantly with homoeostasis model assessment (HOMA) index in nondiabetic RA patients
This study indicates that body mass index, waist, TG, and ratio of TG to high density lipoprotein (HDL) were significantly associated with HOMA index in nondiabetic RA patients

Summary

Introduction

Rheumatoid arthritis (RA) is a complex disease whose pathogenesis remains unknown. Patients with RA have systemic inflammation, as well as increased morbidity and mortality from cardiovascular disease [1, 2]. Various risk factors have been identified that contribute to atherosclerosis in RA patients [3, 4]. Insulin resistance is the most important of these risk factors. Recent years have seen increased attention devoted to inflammation associated insulin resistance [5]. Increasing numbers of research studies illuminate several possible mechanisms, including activation of innate system

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