• Made available online as an Accepted Preprint 24 February 2009
  • Accepted Preprint first posted online on 24 February 2009

Adipokines in the skeleton: influence on cartilage function and joint degenerative diseases

  1. Oreste Gualillo
  1. Research Laboratory 9, (NEIRID LAB, Laboratory of Neuro Endocrine Interactions in Rheumatology and Inflammatory Diseases), Santiago University Clinical Hospital, Calle Choupana s/n, Edificio C, Planta -2, 15706 Santiago de Compostela, Spain
    1Research Laboratory 7 (Molecular and Cellular Cardiology), Santiago University Clinical Hospital, Santiago de Compostela, Spain
    2Department of Physiology, School of Medicine, Santiago University, Santiago de Compostela, Spain
  1. (Correspondence should be addressed to O Gualillo; Email: oreste.gualillo{at}usc.es)


The discovery of leptin in 1994 marked the beginning of a new understanding about white adipose tissue (WAT) and modified a static vision of this tissue which was viewed up to the end of the 20th century as an inert tissue, devoted to body protection from heat loss and to passively storing energy. The identification of the product of the gene obese accentuated the role of adipose tissue in the physiopathology of obesity-linked diseases, and led to the discovery of various adipokines, many of a pro-inflammatory nature. It has become progressively manifest that WAT-derived adipokines can now be considered as the fulcrum between obesity-related environmental causes, such as nutrition and lifestyle, and the biochemical shifts that lead to metabolic syndrome, inflammatory and/or autoimmune conditions, and rheumatic diseases. Herein, we review recent adipokine research, with particular emphasis to the role of leptin, adiponectin, resistin, and visfatin in chondrocyte function and skeleton, as well as in inflammatory and degenerative cartilage joint diseases.

  • Revision received 2 February 2009
  • Accepted 23 February 2009
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