Abstract
Osteosarcopenic obesity (OSO) is a recently identified geriatric syndrome characterized by the concurrent presence of osteopenia/osteoporosis, sarcopenia, and increased adiposity, the latter either as overt overweight or fat redistribution/infiltration into bone and muscle tissues. The diagnostic criteria for OSO are just being established, but there are no data on biomarkers that might characterize this syndrome. Our objective was to examine possible biomarkers associated with OSO syndrome, including serum sclerostin (as a hinder of bone formation via osteoblast inhibition) and skeletal muscle‐specific troponin T (sTnT) (as an indicator of muscle turnover/damage). A total of n=59 healthy Caucasian women ≥65 years were classified into 4 groups based on their bone and body composition profile identified by DXA measurements: 1) Osteopenic/osteoporotic non‐obese with T‐scores of L1–L4 and/or total femur ≤‐1 (N=4); 2) Obese‐only with body fat percentage ≥32 (N=10); 3) Osteopenic/osteoporotic obese (N=35); 4) Osteosarcopenic obese (OSO) (N=10). Sarcopenia was determined from the appendicular lean mass normalized by height and body fat, with the cutoff determined from negative residuals. Serum samples were analyzed using the commercial ELISA kits. Data were evaluated by Pearson's correlations and ANOVA followed by Tukey's tests with p≤0.05. Serum sclerostin concentration ranged from 0.03 to 2.49 ng/mL and was significantly higher in OSO and osteopenic/osteoporotic obese group (1.1 ± 0.2 and 1.09 ± 0.2 ng/mL, respectively) compared to the obese‐only group. The sTnT concentration ranged from 0.02 to 12.06 pg/mL and was also significantly higher in OSO group (3.2 ± 2.9 pg/mL) compared to osteopenic/osteoporotic obese and obese‐only group (1.1 ± 2.2 and 0.6 ± 0.7 pg/mL, respectively). Sclerostin was negatively correlated with bone mineral density/content (BMD/BMC) of all skeletal sites, and the relationship was statistically significant with femoral neck BMD/BMC. Moreover, there was a significant positive correlation between serum sclerostin and sTnT (r=0.3; p≤0.05), indicating their simultaneous mediation in bone and muscle loss. In conclusion, the combination of high sclerostin and sTnT can be used to better identify the metabolic profile of OSO syndrome and possibly apply as measurements for its diagnostic criteria.
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