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THU0081 Role of The Soluble Form of Dipeptydil Peptidase-4(DPP4) in The Insulin Resistance of Patients with Rheumatoid Arthritis
  1. B. Tejera Segura1,
  2. A. de Vera González2,
  3. R. Lopez Mejías3,
  4. B. Ubilla3,
  5. F. Genre3,
  6. J. Olmos4,
  7. J. Hernández4,
  8. J. Llorca5,
  9. M. González-Gay6,
  10. I. Ferraz-Amaro1
  1. 1Division of Rheumatology
  2. 2Central Laboratory Division, Hospital Universitario de Canarias, Santa Cruz de Tenerife
  3. 3Epidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, Rheumatology Division
  4. 4Division of Internal Medicine, Hospital Universitario Marqués de Valdecilla, IDIVAL
  5. 5Division of Epidemiology and Computational Biology, Facultad de Medicina, Universidad de Cantabria y CIBER Epidemiología y Salud Pública (CIBERESP)
  6. 6Division of Rheumatology, Hospital Universitario Marqués de Valdecilla, IDIVAL, Santander, Spain


Background Dipeptidyl peptidase 4 (DPP-4) is an enzyme which plays a fundamental role on glucose homeostasis through degradation of the incretine hormones glucagon like peptide 1 and gastric inhibitory polypeptide.

Objectives To analyze if DPP-4 levels differ between Rheumatoid arthritis (RA) patients and healthy controls, as well as to investigate if they correlate with the insulin resistance (IR) that RA patients express.

Methods 406 subjects, 178 patients with RA and 228 controls adjusted by age and sex, were selected. We determined in both groups glucose, insulin and C peptide levels, Homeostatic Model Assessment (HOMA2) index for insulin and C peptide, and blood levels of the soluble form of DPP-4. We studied with multivariant analysis adjusted for the intake of steroids and other classic factors associated with IR, the differences between patients and controls as well as the correlation of DPP-4 with the activity of the disease and with IR in both groups.

Results Patients had higher levels of insulin (16±26 vs 10±7 microU/mL, p=0,001) and C peptide (1,15±1,02 vs 0,50±0,26 nmol/L, p<0,001) compared to controls. Equivalently, insulin resistance index HOMA-IR (1,81±1,82 vs 1,35±0,93, p=0,002) and HOMA2-IR-peptide C (2,59±2,45 vs 1,10±0,55 nmol/L, p<0,001) were higher in patients with RA. DPP-4 levels were lower in patients with RA than controls (beta coef. -162 [-259–65] ng/ml, p=0.001), after adjustment for age, sex, body mass index and classic factors for IR. Patients with high or moderate activity (633±270 vs 844±757 ng/ml, p=0.06) and low activity (761±340 vs 844±756 ng/ml, p=0.40) had a lower expression of DPP-4 levels compared to those patients in remission, although this difference did not reach statistical significance.

Conclusions Patients with RA express lower levels of DPP-4. This decrease could be explained by the activity of the disease and could play a role in the development of insulin resistance that RA patients express.

Disclosure of Interest None declared

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