Differential expression of leptin and leptin's receptor isoform (Ob-Rb) mRNA between advanced and minimally affected osteoarthritic cartilage; effect on cartilage metabolism

Simopoulou, Theodora; Malizos, Konstantinos N.; Iliopoulos, Dimitrios; Stefanou, Nikolaos; Papatheodorou, Loukia K.; Ιωάννου, Μαρία; Tsezou, Aspasia

doi:10.1016/j.joca.2007.01.018

Cited by 238 publications

(266 citation statements)

References 49 publications

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“…Simopoulou and colleagues investigated the expression of leptin by chondrocytes and observed an increase in leptin messenger RNA in chondrocytes from obese individuals; the increase was not correlated with slightly damaged cartilage but rather, was correlated with advanced OA (19). Leptin treatment of chondrocytes was proinflammatory and catabolic, inducing production of IL-1␤, matrix metalloproteinase 9 (MMP-9), and MMP-13.…”

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confidence: 99%

Obesity and osteoarthritis: Is leptin the link?

Sandell¹

2009

Arthritis & Rheumatism

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There is significant interest in the correlation between adipose regulators of metabolism, inflammation, and the occurrence of osteoarthritis (OA). In this issue of Arthritis & Rheumatism, Griffin and colleagues report the results of their investigation of the role of leptin (1). The investigators hypothesized that obesity in mice resulting from deletion of the leptin gene (ob/ob) or deletion of the leptin receptor gene (db/db) would result in an increased incidence of knee OA, systemic inflammation, and altered subchondral bone morphology. In both of these mouse strains, adiposity was increased by ϳ10-fold compared with controls. Surprisingly, the incidence of OA was not higher in ob/ob and db/db mice than in the control background strain, C57BL/6J mice.These results suggest that obesity alone does not cause OA. However, other changes occurred in these mice due to the loss of leptin function. Leptin-deficient mice had reduced subchondral bone thickness and increased relative trabecular bone volume in the tibial epiphysis, as previously reported (for review, see ref.2). An extensive analysis of inflammatory molecules was carried out by Luminex bead assay, which revealed an increased level of only interleukin-8 (IL-8) and thus not an overall inflammatory effect of leptin deficiency. These results imply that leptin may be involved in the development of OA. Without leptin, adiposity is insufficient to induce systemic inflammation and knee OA, suggesting a potential role of leptin itself in regulating skeletal and immune functions.

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confidence: 99%

Obesity and osteoarthritis: Is leptin the link?

Sandell¹

2009

Arthritis & Rheumatism

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“…Leptin may also trigger cartilage destruction by increasing matrix metalloproteases (MMP)-9 and MMP-13 [26]. The present study shows for first time that there is no significant change in leptin concentration following a cycle of spa therapy.…”

Section: Discussionmentioning

confidence: 52%

“…Leptin induces the expression of growth factors such as IGF-1 and TGF-β1, stimulates proteoglycan and collagen synthesis, and increases the stimulatory effects of proinflammatory cytokines on nitric oxide (NO) production in chondrocytes [23][24][25][26]. Leptin may also trigger cartilage destruction by increasing matrix metalloproteases (MMP)-9 and MMP-13 [26].…”

Section: Discussionmentioning

confidence: 99%

Effects of Spa therapy on serum leptin and adiponectin levels in patients with knee osteoarthritis

et al. 2010

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The aim of the present study was to assess whether spa therapy modified plasma levels of leptin and adiponectin in thirty patients with knee OA treated with a cycle of a combination of daily locally-applied mud packs and bicarbonate-sulphate mineral bath water. Leptin and adiponectin plasma levels were assessed at baseline and after two weeks, upon completion of the spa treatment period. The concentrations of leptin and adiponectin were measured by ELISA.At basal time, plasma leptin levels were significantly correlated with body mass index (BMI) and gender, but no significant correlation was found with patient age, duration of disease, radiographic severity of knee OA, VAS score or Lequesne index.There was no correlation between plasma adiponectin level and BMI, gender and age, duration of the disease, radiographic severity of knee OA, and VAS score. A significant correlation of plasma adiponectin levels was found only with the Lequesne index.At the end of the mud-bath therapy cycle, serum leptin levels showed a slight but not significant increase, while a significant decrease (p<0.05) of serum adiponectin levels was found. However, leptin and adiponectin concentrations after treatment were not correlated with other clinical parameters.In conclusion, our data show that spa therapy can modify plasma levels of the adipocytokines leptin and adiponectin, important mediators of cartilage metabolism. Whether this effect may play a potential role in OA needs further investigations.

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“…The presence of receptors for other adipokines on chondrocytes, synoviocytes, and subchondral osteoblasts (39)(40)(41) does suggest that adipokines may influence joint structure and could be involved with both degenerative and inflammatory processes, from which pain may result. Clinically, adiposity is also associated with tendinopathy (42), and adipokines, such as leptin and adiponectin, have been associated with OA (43,44).…”

Section: Discussionmentioning

confidence: 99%

Association of Fat Mass and Adipokines With Foot Pain in a Community Cohort

Walsh

Gill

Evans

et al. 2016

Arthritis Care & Research

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Objective. To determine, first, if fat mass index (FMI) or fat-free mass index (FFMI) and serum adipokines tumor necrosis factor (TNF) and interleukin-6 (IL-6) are associated with prevalent (stage 2) foot pain, and, second, if they are predictive of future (stage 3) foot pain. Methods. A subset of participants ages ‡50 years (n 5 1,462) from the North West Adelaide Health Study were used for this study. Participants from this community cohort were asked in stage 2 (2004)(2005)(2006) and stage 3 (2008-2010) if they had foot pain, aching, or stiffness. In stage 2, serum adipokines and anthropometry were measured, while body composition was analyzed with dual x-ray absorptiometry. These variables, along with comorbidities and social history, were used in logistic regression analyses to determine if FMI, FFMI, and serum adipokines were associated with foot pain. Results. Prevalent foot pain was present in 20.2% of participants, and future foot pain in 36.4%. Following multivariate modeling, the odds of having pain at stage 2 increased by 8% for each FMI unit (odds ratio [OR] 1.08, 95% confidence interval [95% CI] 1.04-1.12), while the odds of having pain at stage 3 increased by 6% for each FMI unit at stage 2 (OR 1.06, 95% CI 1.02-1.11). TNF level, IL-6 level, and FFMI were not associated with pain. Conclusion. Increased FMI, but not body mass index, FFMI, or TNF or IL-6 level, was associated with both prevalent and future foot pain. These results suggest that body fat may be more important than body weight with respect to foot pain. The role played by other adipokines requires further investigation.

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Differential expression of leptin and leptin's receptor isoform (Ob-Rb) mRNA between advanced and minimally affected osteoarthritic cartilage; effect on cartilage metabolism

Cited by 238 publications

References 49 publications

Obesity and osteoarthritis: Is leptin the link?

Obesity and osteoarthritis: Is leptin the link?

Effects of Spa therapy on serum leptin and adiponectin levels in patients with knee osteoarthritis

Association of Fat Mass and Adipokines With Foot Pain in a Community Cohort

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