Glucosamine is a primary substrate and stimulant of proteoglycan biosynthesis and inhibits the degradation of proteoglycans. Glucosamine may also stimulate synovial production of hyaluronic acid, a compound responsible for the lubricating and shock-absorbing properties of synovial fluid (McCarty 1998, McCarty et al 2000). Glucosamine has been found to cause a statistically significant stimulation of proteoglycan production by chondrocytes from human osteoarthritic cartilage culture (Bassleer et al 1998). Glucosamine sulfate has been also found to modify cultured osteoarthritis chondrocyte metabolism by acting on protein kinase C, cellular phospholipase A2, protein synthesis and possibly collagenase activation (Piperno et al 2000). N-acetyl glucosamine also has been found to produce proliferation of matured cartilaginous tissues and matured cartilage substrate in experimentally produced cartilaginous injuries in rabbits (Tamai et al 2003), and oral administration of glucosamine has been shown to have limited site-specific, partial disease-modifying effect in an animal model of OA (Tiraloche et al 2005). The results of one in-vitro study suggest that the experimental effects of glucosamine are sensitive to the experimental model, the doses and length of treatment and that in the model using bovine chondrocytes pharmacological doses of glucosamine induced a broad impairment in the metabolic activity of the chondrocytes, leading to cell death (de Mattei et al 2002).
Glucosamine was found to have no effect on type 2 collagen fragment levels in serum or urine in a 6-month RCT of 137 subjects with OA of the knee (Cibere et al 2005) and exogenous glucosamine was found not to stimulate chondroitin sulfate synthesis by human chondrocytes in vitro. Furthermore these cells were found to have the capacity to form amounts of glucosamine from glucose far in excess of that provided by levels achievable through oral administration (Mroz & Silbert 2004).
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