TY - JOUR T1 - Is Visceral Fat the Missing Link in the Relationship Between Inflammation and Insulin Resistance in RA? JF - The Journal of Rheumatology JO - J Rheumatol SP - 1906 LP - 1909 DO - 10.3899/jrheum.140780 VL - 41 IS - 10 AU - MICHELLE J. ORMSETH AU - C. MICHAEL STEIN Y1 - 2014/10/01 UR - http://www.jrheum.org/content/41/10/1906.abstract N2 - Several groups of investigators evaluating insulin resistance in rheumatoid arthritis (RA; Table 1)1,2,3,4,5,6,7,8,9 have reported that patients with RA have more insulin resistance than non-RA control subjects, even with similar body mass index (BMI)1,2,3,4,5. In many RA studies, insulin resistance was associated with markers of inflammation or disease activity5,6,7,8. Moreover, some studies that examined insulin resistance before and after treatment of RA with anti-tumor necrosis factor-α (TNF-α) or antiinterleukin 6 (IL-6) agents found that treatment with these drugs, and presumably the consequent decrease in inflammation, resulted in a significant improvement in insulin sensitivity10,11. These and other studies provide support for the notion that inflammation in RA promotes insulin resistance.View this table:In this windowIn a new windowTable 1. Select publications evaluating insulin resistance in RA versus non-RA control subjects.The concept that there is a relationship between the inflammation in RA and insulin resistance is also supported by studies performed in animals showing that inflammation promotes insulin resistance. For example, administration of TNF-α and IL-6 caused insulin resistance in rats and mice12,13. This finding is not surprising because cytokines such as IL-6 and TNF-α contribute to insulin resistance through downstream repression of insulin signaling (reviewed14).In this issue of The Journal, AbouAssi and colleagues present a meticulous and thorough evaluation of insulin sensitivity in 39 patients with RA and 39 control subjects matched for not only age and sex, but also for BMI and physical activity15. Insulin sensitivity was quantified by frequently sampled intravenous glucose … Address correspondence to Dr. Ormseth, 1161 21st Ave. South, T-3113 MCN, Nashville, Tennessee 37232-2681, USA; E-mail: michelle.ormseth{at}vanderbilt.edu ER -