Vince
Super Moderator
Circulating leptin was linked to knee cartilage thinning in adults after adjusting for body mass index and other factors, and may potentially explain the association between obesity and cartilage thickness.
Over 2.7 years, baseline levels of leptin and changes in leptin over time were negatively associated with changes in medial tibial cartilage thickness in a cohort of 163 subjects older than 50, reported Oliver P. Stannus, of the University of Tasmania in Australia, and colleagues in Annals of Rheumatic Diseases.
Leptin is a protein that influences body weight homeostasis and regulates immune and inflammatory processes. A previous study using magnetic resonance imaging (MRI) found serum leptin to be associated with reduced knee cartilage volume. Because cartilage thickness may be more sensitive in detecting early osteoarthritis (OA), the authors sought to determine the cross-sectional and longitudinal associations between serum leptin levels and knee cartilage thickness. The 163 subjects were selected randomly from the Tasmanian Older Adult Cohort study, which sought to identify factors related to development and progression of OA. All had MRI images of the right knee at baseline and follow-up to assess knee cartilage thickness, and 157 had serum leptin measurements at baseline and follow-up for longitudinal analysis.
Forty-six percent of the participants were women; average age of the entire cohort at baseline was 62.6 years and their mean body mass index (BMI) was 27.5. The median and mean leptin levels were 8.65 pg/mL and 12.69 pg/mL, respectively.
Cross-sectional analyses showed that leptin levels were significantly associated with knee cartilage thickness at all sites: femoral (beta -0.013, 95% CI minus 0.022-minus 0.003), medial tibial (beta -0.009, 95% CI minus 0.018-minus -0.001), lateral tibial (beta -0.012, 95% CI minus 0.021-minus 0.003), and patellar (beta -0.014, 95% CI minus 0.026 -minus 0.002) after adjustment for age, sex, BMI, radiographic OA, lean mass, and smoking and disease status.
Longitudinally, baseline leptin was negatively associated with change in cartilage thickness at the femoral, medial tibial, and lateral tibial sites, and the association with change in medial tibial cartilage thickness (beta -0.004, 95% CI minus 0.007-minus 0.001) remained significant after adjustment for the same covariates above. Change in serum leptin was negatively associated with change in medial tibial cartilage thickness, and this association remained unchanged after multivariable analysis (beta -0.009, 95% CI minus 0.018-minus 0.001).
Excess leptin may play a catabolic role that contributes to the pathological process of OA, the authors speculate. In animal studies, it appeared to be an important local and systemic factor that influences cartilage degradation. Decreases in serum leptin with weight loss may explain the improvement in physical function and symptoms in patients with knee OA who lose weight.
Two other features of leptin in OA may have been elucidated in the current study. "First, adiposity status as a risk factor for OA may be mediated by leptin," as participants with higher baseline levels of leptin had higher BMI, total body fat and trunk fat, and lower cartilage thickness than those with lower levels of leptin, the authors wrote. "We also found significant associations between adiposity measures and cartilage thickness, the magnitude of which decreased substantially at all sites after adjustment for leptin, providing support for this hypothesis of mediation."
Second, longitudinal results demonstrated that loss of media tibial cartilage thickness was most strongly associated with leptin, which may indicate that cartilage degradation is more common in the medial compartment.
The response rate of only 57% yielded a modest sample size, which represents a possible limitation, the authors note, but was offset by a high retention rate (82%). Comorbidities in the sample may have affected the associations, even though results were largely unchanged when adjusted for disease status or when subjects with other diseases were excluded from analysis. Also, leptin levels measured in serum do not allow for detection of local autocrine or paracrine effects of leptin.
http://www.medpagetoday.com/Rheumatology/Arthritis/49262
Over 2.7 years, baseline levels of leptin and changes in leptin over time were negatively associated with changes in medial tibial cartilage thickness in a cohort of 163 subjects older than 50, reported Oliver P. Stannus, of the University of Tasmania in Australia, and colleagues in Annals of Rheumatic Diseases.
Leptin is a protein that influences body weight homeostasis and regulates immune and inflammatory processes. A previous study using magnetic resonance imaging (MRI) found serum leptin to be associated with reduced knee cartilage volume. Because cartilage thickness may be more sensitive in detecting early osteoarthritis (OA), the authors sought to determine the cross-sectional and longitudinal associations between serum leptin levels and knee cartilage thickness. The 163 subjects were selected randomly from the Tasmanian Older Adult Cohort study, which sought to identify factors related to development and progression of OA. All had MRI images of the right knee at baseline and follow-up to assess knee cartilage thickness, and 157 had serum leptin measurements at baseline and follow-up for longitudinal analysis.
Forty-six percent of the participants were women; average age of the entire cohort at baseline was 62.6 years and their mean body mass index (BMI) was 27.5. The median and mean leptin levels were 8.65 pg/mL and 12.69 pg/mL, respectively.
Cross-sectional analyses showed that leptin levels were significantly associated with knee cartilage thickness at all sites: femoral (beta -0.013, 95% CI minus 0.022-minus 0.003), medial tibial (beta -0.009, 95% CI minus 0.018-minus -0.001), lateral tibial (beta -0.012, 95% CI minus 0.021-minus 0.003), and patellar (beta -0.014, 95% CI minus 0.026 -minus 0.002) after adjustment for age, sex, BMI, radiographic OA, lean mass, and smoking and disease status.
Longitudinally, baseline leptin was negatively associated with change in cartilage thickness at the femoral, medial tibial, and lateral tibial sites, and the association with change in medial tibial cartilage thickness (beta -0.004, 95% CI minus 0.007-minus 0.001) remained significant after adjustment for the same covariates above. Change in serum leptin was negatively associated with change in medial tibial cartilage thickness, and this association remained unchanged after multivariable analysis (beta -0.009, 95% CI minus 0.018-minus 0.001).
Excess leptin may play a catabolic role that contributes to the pathological process of OA, the authors speculate. In animal studies, it appeared to be an important local and systemic factor that influences cartilage degradation. Decreases in serum leptin with weight loss may explain the improvement in physical function and symptoms in patients with knee OA who lose weight.
Two other features of leptin in OA may have been elucidated in the current study. "First, adiposity status as a risk factor for OA may be mediated by leptin," as participants with higher baseline levels of leptin had higher BMI, total body fat and trunk fat, and lower cartilage thickness than those with lower levels of leptin, the authors wrote. "We also found significant associations between adiposity measures and cartilage thickness, the magnitude of which decreased substantially at all sites after adjustment for leptin, providing support for this hypothesis of mediation."
Second, longitudinal results demonstrated that loss of media tibial cartilage thickness was most strongly associated with leptin, which may indicate that cartilage degradation is more common in the medial compartment.
The response rate of only 57% yielded a modest sample size, which represents a possible limitation, the authors note, but was offset by a high retention rate (82%). Comorbidities in the sample may have affected the associations, even though results were largely unchanged when adjusted for disease status or when subjects with other diseases were excluded from analysis. Also, leptin levels measured in serum do not allow for detection of local autocrine or paracrine effects of leptin.
http://www.medpagetoday.com/Rheumatology/Arthritis/49262
