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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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