Session Type: Abstract Submissions (ACR)
Rheumatoid arthritis (RA) is associated with a high prevalence of insulin resistance. Most prior investigations of insulin resistance in RA have examined fasting glucose and insulin. However, because glucose uptake is performed predominantly by skeletal muscle, skeletal muscle insulin resistance is best assessed with a glucose challenge. We determined if persons with RA exhibit more skeletal muscle insulin resistance than age, gender, race, and BMI–matched controls, and if inflammation, inactivity, and low dose prednisone use mediated skeletal muscle insulin resistance.
We enrolled 50 participants with RA and 50 matched controls; all had no history of diabetes or cardiovascular disease. The patients with RA had not changed their anti-rheumatic therapy in the previous 3months and may have been taking low doses of prednisone (5 mg or less per day); any steroid tapers were completed at least three weeks prior to study enrollment. Participants completed questionnaires for medication information, a visual analog scale for health rating, and the Stanford Brief Activity Survey for physical activity. Each underwent anthropomorphic measures, a 28 joint exam, and fasting blood collection for glucose, insulin, and an erythrocyte sedimentation rate (ESR), used to compute a disease activity score (DAS-28). Fasting glucose and insulin were used to calculate the Homeostasis Model of Assessment (HOMA). A frequently-sampled intravenous glucose tolerance test was performed with glucose and insulin measured in each sample. Bergman’s minimal model was used to determine insulin sensitivity (SI), indicative of skeletal muscle insulin sensitivity. SI was logarithmically transformed prior to group comparisons with a t-test and predictor identification with linear modeling.
Persons with RA reported less physical activity (P=0.046) than controls, and had a slightly higher median (IQR) ESR [4 (1, 5) vs. 8 (1, 18) mm/h, P=0.05]. The median (IQR) DAS-28 was 2.9 (2.1, 3.8). Daily low dose prednisone use was reported by 27%.
Persons with RA were more insulin resistant than controls (geometric mean (SD) 4.4 (2.39) versus 4.8(2.1)*10-5min-1/[pmol/l]), but this difference was not statistically significant (P=0.37). Prednisone use was related to SI independent of the contributions of BMI, fasting insulin, HOMA, gender and physical activity (R2 = 0.56, model P<0.0001, prednisone use, partial R2=0.10, P=0.03). Prednisone use was associated with more than a 41% lower SI. There was a trend for an independent relation for physical activity with SI (partial R2=0.03, P=0.09). Age, ESR, DAS-28, NSAID, DMARD, or biologic use did not contribute to SI in the aforementioned model.
Although persons with RA showed higher insulin resistance, this difference did not achieve statistical significance. However, in persons with RA, the use of low dose prednisone therapy did appear to increase skeletal muscle insulin resistance independent of BMI and physical activity. Future studies should determine if interventions, such as regular physical activity, can counteract the effect of low dose prednisone use on skeletal muscle insulin resistance.
G. E. McDaniel,
E. W. St. Clair,
W. E. Kraus,
K. M. Huffman,
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ACR Meeting Abstracts - https://acrabstracts.org/abstract/contributions-of-inflammation-inactivity-and-low-dose-prednisone-use-to-skeletal-muscle-insulin-resistance-in-well-controlled-rheumatoid-arthritis/