Research Updates: Do glucosamine-based chondroprotective agents affect fructosamine monitoring in diabetic dogs?


Research Updates: Do glucosamine-based chondroprotective agents affect fructosamine monitoring in diabetic dogs?

Dec 01, 2010

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Glucosamine is a precursor of glycosaminoglycans, a major component of normal cartilage matrix. Supplementation with a combination of glucosamine and chondroitin sulfate ameliorates signs of osteoarthritis in dogs and people and is commonly prescribed to veterinary patients with suspected or confirmed degenerative joint disease. However, because glucosamine is composed of glucose and glutamine, administration of such chondroprotective agents could, in theory, increase serum glucose concentrations and thereby increase an animal's insulin requirements even further or, alternatively, could be contributing to pancreatic beta cell death by worsening hyperglycemia-associated glucose toxicity.

Fructosamine, which is formed by the nonenzymatic glycosylation of albumin, is often measured when monitoring insulin therapy in diabetic dogs. Increases in serum fructosamine concentration in most cases are due to sustained hyperglycemia, so results above the reference range in a diabetic patient usually imply inadequate insulin dosing. The goal of this study was, therefore, to determine the impact of oral glucosamine-chondroitin sulfate supplementation on fructosamine concentrations in healthy dogs and, thereby, provide preliminary data on whether clinicians should consider the impact of this agent on monitoring protocols in diabetic patients.

Twelve healthy adult dogs were enrolled in this prospective, blinded, crossover study. Dogs fed a therapeutic diet designed to treat joint disease were excluded from enrollment because these diets may contain an undetermined amount of glucosamine. Six dogs (group 1) were randomly allocated to receive glucosamine-chondroitin sulfate once daily at the manufacturer's recommended dose for three weeks, and six dogs (group 2) were randomly allocated to receive a placebo (microcrystalline cellulose) once daily incorporated into an identical capsule for three weeks. Serum fructosamine concentrations were measured in all dogs before and at the end of the treatment period.

After completion of the first three-week study period, the glucosamine-chondroitin sulfate and placebo were discontinued in all dogs, and following a four-week washout period, group 1 dogs were then administered the placebo for three weeks, while group 2 dogs received the chondroprotective agent, again with measurement of serum fructosamine concentrations before and after treatment. Statistical analysis revealed that there was no difference in mean fructosamine concentrations before or after administration of glucosamine-chondroitin sulfate or placebo, and no significant difference was seen between fructosamine concentrations observed in dogs receiving the chondroprotective agent vs. the placebo.