ArticleArthritis research & therapy2010
Obesity affects the chondrocyte responsiveness to leptin in patients with osteoarthritis.
Article in Arthritis research & therapy, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 78 citations in OpenAlex.
- Effects of glucosamine sulfate and exercise therapy on serum leptin levels in patients with knee osteoarthritis: preliminary results of randomized controlled clinical trial.Rheumatology international · 2013Trial
- Adipose-Joint Crosstalk in Obesity-Induced Osteoarthritis: Mechanisms, Biomarkers, and Translational Therapeutic Opportunities.Current rheumatology reports · 2026Review
- Obesity-induced fibrosis in osteoarthritis: Pathogenesis, consequences and novel therapeutic opportunities.Osteoarthritis and cartilage open · 2024Review
- Novel perspectives on leptin in osteoarthritis: Focus on aging.Genes & diseases · 2024Review
- Effects of Leptin and Body Weight on Inflammation and Knee Osteoarthritis Phenotypes in Female Rats.JBMR plus · 2023Article
- Fundamentals of OA. An initiative of Osteoarthritis and Cartilage. Obesity and metabolic factors in OA.Osteoarthritis and cartilage · 2022Review
- Protective effect of ethanolic extract of Echinacea purpurea contained nanoparticles on meniscal/ligamentous injury induced osteoarthritis in obese male rats.Scientific reports · 2022Article
- Concentration of Selected Metalloproteinases and Osteocalcin in the Serum and Synovial Fluid of Obese Women with Advanced Knee Osteoarthritis.International journal of environmental research and public health · 2022Article
- Adipokine Signaling Pathways in Osteoarthritis.Frontiers in bioengineering and biotechnology · 2022Review
- The Effect of Body Mass Index and Metformin on Matrix Gene Expression in Arthritic Primary Human Chondrocytes.Cartilage · 2021Article
- eNAMPT Is Localised to Areas of Cartilage Damage in Patients with Hip Osteoarthritis and Promotes Cartilage Catabolism and Inflammation.International journal of molecular sciences · 2021Article
- Article
- Cartilage tissue engineering for obesity-induced osteoarthritis: Physiology, challenges, and future prospects.Journal of orthopaedic translation · 2021Review
- Quality of life, function and disability in individuals with chronic ankle symptoms: a cross-sectional online survey.Journal of foot and ankle research · 2020Article
- Metabolic syndrome and subchondral bone alterations: The rise of osteoarthritis - A review.Journal of clinical orthopaedics and trauma · 2020Article
- Long noncoding RNA LINC00461 induced osteoarthritis progression by inhibiting miR-30a-5p.Aging · 2020Article
- Adipokines: New Therapeutic Target for Osteoarthritis?Current rheumatology reports · 2019Review
- Sphingolipids in Obesity and Correlated Co-Morbidities: The Contribution of Gender, Age and Environment.International journal of molecular sciences · 2019Review
- miR-137 suppresses cell growth and extracellular matrixdegradation through regulating ADAMTS-5 in chondrocytes.American journal of translational research · 2019Article
- Adipokines and inflammation: is it a question of weight?British journal of pharmacology · 2018Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionIncreasing evidence support the regulatory role of leptin in osteoarthritis (OA). As high circulating concentrations of leptin disrupt the physiological function of the adipokine in obese individuals, the current study has been undertaken to determine whether the elevated levels of leptin found in the joint from obese OA patients also induce changes in the chondrocyte response to leptin.
methodsChondrocytes isolated from OA patients with various body mass index (BMI) were treated with 20, 100 or 500 ng/ml of leptin. The expression of cartilage-specific components (aggrecan, type 2 collagen), as well as regulatory (IGF-1, TGFbeta, MMP-13, TIMP 2) or inflammatory (COX-2, iNOS, IL-1) factors was investigated by real-time PCR to evaluate chondrocyte responsiveness to leptin. Furthermore, the effect of body mass index (BMI) on leptin signalling pathways was analyzed with an enzyme-linked immunosorbent assay for STATs activation.
resultsLeptin at 20 ng/ml was unable to modulate gene expression in chondrocytes, except for MMP-13 in obese OA patients. Higher leptin levels induced the expression of IGF-1, type 2 collagen, TIMP-2 and MMP-13. However, the activity of the adipokine was shown to be critically dependent on both the concentration and the BMI of the patients with a negative association between the activation of regulated genes and BMI for 100 ng/ml of adipokine, but a positive association between chondrocyte responsiveness and BMI for the highest leptin dose. In addition, the gene encoding MMP-13 was identified as a target of leptin for chondrocytes originated from obese patients while mRNA level of TIMP-2 was increased in leptin-treated chondrocytes collected from normal or overweight patients. The adipokine at 500 ng/ml triggered signal transduction through a STAT-dependent pathway while 100 ng/ml of leptin failed to activate STAT 3 but induced STAT 1alpha phosphorylation in chondrocytes obtained from obese patients.
conclusionsThe current study clearly showed that characteristics of OA patients and more especially obesity may affect the responsiveness of cultured chondrocytes to leptin. In addition, the BMI-dependent effect of leptin for the expression of TIMP-2 and MMP-13 may explain why obesity is associated with an increased risk for OA.
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