Horm Metab Res 2011; 43(11): 801-808
DOI: 10.1055/s-0031-1287783
Humans, Clinical
© Georg Thieme Verlag KG Stuttgart · New York

Systemic Blockade of TNF-α does not Improve Insulin Resistance in Humans

Authors

  • I. Ferraz-Amaro

    1   Servicio de Reumatología, Hospital Universitario de Canarias, La Laguna, Santa Cruz de Tenerife, Spain
  • M. Arce-Franco

    1   Servicio de Reumatología, Hospital Universitario de Canarias, La Laguna, Santa Cruz de Tenerife, Spain
  • J. Muñiz

    2   IMETISA, Hospital Universitario de Canarias, La Laguna, Santa Cruz de Tenerife, Spain
  • J. López-Fernández

    3   Servicio de Endocrinología, La Laguna, Santa Cruz de Tenerife, Spain
    4   Departamento de Medicina, Facultad de Medicina, Universidad de La Laguna, La Laguna, Santa Cruz de Tenerife, Spain
  • V. Hernández-Hernández

    1   Servicio de Reumatología, Hospital Universitario de Canarias, La Laguna, Santa Cruz de Tenerife, Spain
  • A. Franco

    5   Laboratorio de Inmunología, Hospital Universitario de Canarias, La Laguna, Santa Cruz de Tenerife, Spain
  • J. Quevedo

    6   Servicio de Reumatología, Hospital Universitario Dr. Negrin, Las Palmas de Gran Canarias, Spain
  • J. Martínez-Martín

    7   Servicio de Endocrinología, Hospital Universitario Dr. Negrin, Las Palmas de Gran Canarias, Spain
  • F. Díaz-González

    1   Servicio de Reumatología, Hospital Universitario de Canarias, La Laguna, Santa Cruz de Tenerife, Spain
    4   Departamento de Medicina, Facultad de Medicina, Universidad de La Laguna, La Laguna, Santa Cruz de Tenerife, Spain
Further Information

Publication History

received 03 July 2011

accepted 26 August 2011

Publication Date:
18 October 2011 (online)

Preview

Abstract

The purpose of this study was to determine whether long-term modulation of inflammatory activity by tumor necrosis factor (TNF)-α inhibitors has some influence on insulin resistance (IR). 16 active rheumatoid arthritis (RA) patients without CV risk factors treated with anti-TNF-α agents were included in this study. RA activity by disease activity score 28, IR by HOMA2-IR, body composition by impedance analysis, physical activity by accelerometry, abdominal fat distribution by magnetic resonance imaging, and serum level of key adipokines by ELISA were measured at baseline and during a 1-year follow-up period. Patient body mass index increased significantly (26.94±3.88 vs. 28.06±4.57 kg/m2, p=0.02) after 1 year of treatment. Body composition, in terms of fat and fat-free mass, remained unchanged except for a significant elevation in body cell mass (25.50±4.60 vs. 26.60±3.17 kg, p=0.02). Basal levels of IR in the RA patients included in this study were significantly higher than healthy controls (1.6±0.8 vs. 1.11±0.56, p=0.011) but did not change during the follow-up. Nor did basal concentrations of adiponectin, visfatin, leptin, ghrelin, resistin, and apelin in response to anti-TNF-α treatment; only retinol-binding protein 4, showed a significant increase (51.7±32.7 vs. 64.9±28.4 μg/ml, p=0.03) at the end of the study. IR, adiposity distribution, and serum levels of most adipokines are not significantly affected by long-term inhibition of TNF-α in RA patients. Our data suggest that although systemic blockade of TNF-α exerts an anticachectic effect in RA patients, it does not seem to play a major role in IR.