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.
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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.