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A randomized double‑blind placebo‑controlled clinical study was conducted to evaluate the chondroprotective action of glucosamine on healthy subjects (soccer players) without joint disorders. Collegiate soccer players (n=43) without joint disorders were randomly assigned to receive a glucosamine (2 g/day)‑containing supplement (n=22, glucosamine group) or a placebo (n=21, placebo group) for 16 weeks, and cartilage metabolism was evaluated by analyzing markers for type II collagen degradation urine C‑terminal telopeptide‑II (CTX‑II) and serum collagen type II cleavage (C2C) and synthesis urine C-terminal type II procollagen peptide (CPII). In the initial analysis of all subjects, urine CTX‑II level substantially decreased in the glucosamine group, but not in the placebo group after the intervention for 16 weeks (P=0.05). Moreover, CTX‑II level in the glucosamine group was also significantly lower than that in the placebo group at week 16 during the intervention. In the second analysis, to make the effect of the test supplement more clear, 41 subjects with less variation of exercise loading were evaluated. The results revealed that urine CTX‑II level significantly decreased in the glucosamine group (n=21), but not in the placebo group (n=20) after the intervention (P<0.05). Moreover, CTX‑II levels in the glucosamine group significantly decreased compared with the placebo group after the intervention (P<0.05). Both in the initial and second analyses, serum C2C level significantly decreased in the glucosamine group, but not in the placebo group after the intervention (P<0.05). In contrast, urine CPII level was not significantly changed even after the intervention in both the placebo and glucosamine groups. Importantly, no test supplement‑related adverse events were observed. These observations suggest that oral administration of glucosamine (2 g/day for 16 weeks) exerts a chondroprotective action on healthy subjects (soccer players) without joint disorders. This effect was achieved by improving cartilage metabolism (suppressing type II collagen degradation but maintaining type II collagen synthesis), without causing apparent adverse effects.

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http://dx.doi.org/10.3892/mmr.2018.9396DOI Listing

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