Glucosamine, 2-amino-2-deoxy-D-glucose, is an amino monosaccharide that is an essential component of mucopolysaccharides and chitin. Glycosaminoglycans (mucopolysaccharides) are large complexes of negatively-charged carbohydrate chains that are incorporated into mucous secretions, connective tissue, skin, tendons, ligaments and cartilage. Glucosamine and its acetylated derivative, N-acetylglucosamine, are readily synthesized in the body from glucose. Because of its high concentration in joint tissues, the hypothesis that glucosamine supplements would provide symptomatic relief for osteoarthritis was developed more than 30 years ago (D’Ambrosio et al., 1981). Many clinical trials have tested this hypothesis (Institute of Medicine, 2004) and glucosamine supplements are widely used to relieve arthritic complaints (Houpt et al., 1999).
To meet the demand for glucosamine nutritional supplements, three forms of glucosamine are commonly available: glucosamine hydrochloride, glucosamine sulfate, and N-acetyl-glucosamine. These glucosamine compounds are generally derived from chitin, a biopolymer present in the exoskeleton of marine invertebrate animals. The glucosamine derived from chitin in the cell walls of many fungi appears to be chemically identical to that found in marine invertebrates (Institute of Medicine, 2004).
This report is a critical evaluation of the available information on the safety of glucosamine in animals and humans and its effects on glucose metabolism. The effects of glucosamine intake on blood, urine, and fecal parameters, blood pressure and pulse rate and reported side effects are summarized. NSAID are widely prescribed and purchased over-the-counter for osteoarthritic complaints but have significant side effects and are associated with >16,000 deaths annually in the US (Wolfe et al., 1999). The efficacy and safety of glucosamine for arthritic complaints will be compared to other oral preparations.
Contents
1. Introduction
2. Biological effects
2.1. Absorption, distribution, metabolism and excretion (ADME)
2.2. Biochemical pathways
3. Animal toxicity
3.1. Acute oral toxicity
3.2. Subchronic and chronic oral toxicity
3.3. Toxicity by the parenteral route
3.4. In vitro studies
3.5. Mutagenicity data
- 3.5.1. In vitro studies
3.5.2. In vivo studies
4. Human clinical studies
4.1. Clinical trial selection
4.2. Characteristics of clinical studies
4.3. Effects of glucosamine on glucose metabolism in humans
4.4. Objective measures of safety
4.5. Common symptoms with placebo, glucosamine and NSAID
4.6. Assessment of efficacy
5. Discussion
6. Conclusions
Acknowledgments
References
