Evaluation of the effect of the administration of an N-acetyl-glucosamine-containing green tea supplement on biomarkers for cartilage metabolism in healthy individuals without symptoms of arthritis: a randomized double-blind placebo-controlled clinical study

Background: To evaluate the chondroprotective action of an N-acetyl-glucosamine (GlcNAc)-containing supplement on the joint health of healthy individuals without symptoms of arthritis, we conducted a randomized double-blind placebo-controlled clinical trial. Methods: Subjects (n=100, 51.3 +/- 1.0 years (mean +/- SE)) without symptoms of arthritis were randomly assigned to receive a 1000 mg GlcNAc-containing diet (GlcNAc group) or a placebo diet (placebo group) once a day for 16 weeks, and the effect on the cartilage metabolism was evaluated by analyzing the ratio of type II collagen degradation to synthesis using type II collagen degradation (C2C) and synthesis (PIICP) markers. Results: The results indicated that the changes in the C2C/PIICP ratios from the baseline were slightly suppressed in the GlcNAc group compared with those in the placebo group at weeks 16 during the intervention and 4 weeks after the intervention. However, there was no significant difference between the two groups. To make the effect of GlcNAc even more clear, the subjects with joint loading and impaired cartilage metabolism were evaluated. Interestingly, the changes in the C2C/PIICP ratios from the baseline were significantly suppressed in the GlcNAc group compared with the placebo group at weeks 16 during the intervention and 4 weeks after the intervention. Moreover, test supplement-related adverse events were not essentially observed during and after the intervention. Conclusions: These observations suggest that the oral administration of GlcNAc at a dose of 1000 mg/day exerts a chondroprotective action on the healthy individuals by lowering the C2C/PIICP ratio, which indicates relative reduction of type II collagen degradation and increase of type II collagen synthesis, without apparent adverse effect.