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Expression and modulation of adipolin/C1qdc2: a novel adipokine in human and murine ATDC-5 chondrocyte cell line
  1. Javier Conde1,
  2. Morena Scotece1,
  3. Verónica López1,
  4. Rodolfo Gómez1,
  5. Francisca Lago2,
  6. Jesús Pino3,
  7. Juan Jesús Gómez-Reino1,
  8. Oreste Gualillo1
  1. 1SERGAS, Research Laboratory 9, NEIRID Lab (Neuroendocrine Interactions in Rheumatology and Inflammatory Diseases), Institute of Medical Research (IDIS), Santiago University Clinical Hospital, Santiago de Compostela, Spain
  2. 2SERGAS, Research Laboratory 7 (Molecular and Cellular Cardiology), Institute of Medical Research (IDIS), Santiago University Clinical Hospital, Santiago de Compostela, Spain
  3. 3SERGAS, Division of Orthopaedics Surgery and Traumatology, Santiago University Clinical Hospital,Santiago de Compostela, Spain
  1. Correspondence to Dr Oreste Gualillo, SERGAS, Research Laboratory 9, NEIRID Lab (Neuroendocrine Interactions in Rheumatology and Inflammatory Diseases), Institute of Medical Research (IDIS), Santiago University Clinical Hospital, Travesia Choupana s/n, Building C, Level-2, Santiago de Compostela 15706, Spain; oreste.gualillo{at}sergas.es

https://doi.org/10.1136/annrheumdis-2012-201693

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    Osteoarthritis (OA) is the most frequent articular disease, characterised by the irreversible loss of articular cartilage and accompanied by changes in the synovium and subchondral bone.1 Chondrocytes are the unique cell type of adult articular cartilage capable of maintaining cartilage components under normal turnover conditions.2

    Several factors affect the normal physiology of chondrocytes including mechanical stress, proinflammatory cytokines and obesity.3 The latter is characterised by a dysfunction of adipose tissue and its adipokine secretion pattern, indicating that metabolic changes as a result of obesity may have an additional aetiological influence on OA susceptibility, phenotype and progression. Adipokines such as leptin and adiponectin affect articular cartilage degradation by inducing proinflammatory factors such as interleukin (IL)-6, nitric oxide and IL-8 at the cartilage level.4 ,5 The role of adipokines in joint homeostasis is currently under investigation, but it is a matter of debate since some clinical studies have not been able to identify major involvement of adipokines in OA.

    C1qdc2/CTRP12, also called adipolin (adipose-derived insulin-sensitising factor), is a very recently described adipokine which is abundantly expressed in adipose tissue.6 This novel adipokine is decreased in rodent obesity models. Adipolin ameliorates glucose intolerance and insulin resistance in diet-induced obese mice.6 ,7 In addition, …

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    Footnotes

    • Contributors JC participated in acquisition of data, analysis and interpretation of data and critical revision of the manuscript. MS, VL, JP and RG participated in acquisition of data, drafting of the manuscript and statistical analysis. JJG-R participated in analysis and interpretation of data and drafting of the manuscript. OG and FL participated in conception and design of the study, analysis and interpretation of data, critical revision of the manuscript and scientific supervision of experiments.

    • Funding The work of OG and FL is funded by the Instituto de Salud Carlos III and the Xunta de Galicia (SERGAS) through a research staff stabilisation contract. This work was also partially supported by RETICS Programme, RD08/0075 (RIER) from Instituto de Salud Carlos III (ISCIII) within the VI NP of R+D+I 2008–2011.

    • Competing interests None.

    • Ethics approval This study was conducted with the approval of the Santiago University Clinical Hospital ethics committee.

    • Provenance and peer review Not commissioned; externally peer reviewed.