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Glucosamine is an abundant monosaccharide and a prominent precursor in the biochemical synthesis of glycosylated proteins and lipids (Fig. 1a). Glucosamine is also a structural part of the polysaccharides chitosan and chitin, which compose the exoskeletons of crustaceans and other arthropods, as well as the cell walls of fungi and many higher organisms. The hydrolysis of crustacean exoskeletons or, less commonly, by fermentation of a grain such as corn or wheat, is used to produce glucosamine commercially. In the USA, glucosamine is one of the most common non-vitamin, non-mineral, dietary supplements used by adults and is considered a " dietary supplement " (food) rather than a drug. To market any dietary supplement as a treatment for any disease or condition is illegal in the USA. The US National Institutes of Health funded a 24-week, 12.5 million-dollar multicenter clinical trial, the Glucosamine/Chondroitin Arthritis Intervention Trial (GAIT), to study the effect of chondroitin sulfate, glucosamine hydrochloride, chondroitin/glucosamine in combination, and celecoxib as a treatment for knee pain in two groups of patients with osteoarthritis of the knee. The GAIT study could show no effectiveness for glucosamine [1]. Cochrane reviews, other meta-analyses, and other studies reached similar conclusions [2]. Thus, a healthy dose of skepticism (caveat emptor) is warranted when inspecting the salubrious effects of glucosamine on health. The glucosamine focus has been on osteoarthritis where loss of collagen surfaces is the major issue but fibrosis and scarring also play a role. Chronic fibrosis also involves the kidney. Indeed, urinary tract obstruction leads to renal fibrosis and the unilateral ureteral obstruction (UUO) model is a favorite of investigators, since the opposite kidney is an ideal non-obstructed control. Fibrosis and scarring are complicated conditions involving a host of pathways; however, the transforming growth factor-β (TGF-β) is very commonly implicated [3]. Inhibiting TGF-β1 to avoid fibrosis in the kidney has been discussed for 25 years [4]. Unfortunately, translating laboratory findings to the clinical arena has not been very successful. In an earlier study [5], investigators from the same laboratory as the current report observed that inhibiting the N-linked glycosylation process impedes binding of TGF-β1 to the TβRII receptor complex and thereby render cells resistant to TGF-β signaling (Fig. 1b). The human embryonic kidney-293 cell line exhibited reduced TGF-β signaling when either treated with tunicamycin that inhibits N-linked glycosylation or another endoplasmic reticulum inhibitor. The authors reported that defective N-linked glycosylation prevented TβRII proteins from being …

Glucosamine and caveat emptor