This study demonstrated that short-term administration of glucosamine-chondroitin sulfate does not significantly affect serum
fructosamine concentrations in healthy dogs. Although a previous study had determined that administration of a chondroprotective
agent to healthy dogs for 30 days does not increase serum glucose concentration,1 direct confirmation that serum fructosamine concentrations were likewise unaffected was necessary because of the effects
of this class of drugs on glucose homeostasis in different mammalian species.
For example, glucosamine induces insulin resistance in rats but not in healthy people or those with type 2 diabetes mellitus,2 likely because the conversion of glucose and glutamine to glucosamine is irreversible in humans and is, therefore, unlikely
to result in hyperglycemia2 ; whether or not the same is true in dogs is unknown.
Because of this uncertainty, one could theorize, for example, that if glucosamine-derived serum glucose in dogs were to somehow
be preferentially and rapidly bound to serum albumin, this would result in normal serum glucose but increased serum fructosamine
concentrations. Therefore, any suggested redundancy of this study with previous investigations of glucose homeostasis in dogs
administered chondroitin-based supplements is not justified.
Despite this justification for directly determining whether fructosamine concentrations are affected by short-term administration
of glucosamine-chondroitin sulfate, two important limitations of this study prevent definitively stating that glucosamine-chondroitin
sulfate supplements will have no effect on glucose homeostasis. First, the effect of this supplement on serum fructosamine
concentrations was studied in healthy dogs rather than in dogs with diabetes mellitus. Several metabolic pathways (i.e. not just glucose homeostasis) are altered in patients with this disease, and, as such, glucosamine catabolism and biologic
activity of any drug metabolites could in theory differ between these two populations. Second, chondroprotective agents are
often administered for months to years rather than the 30-day period described in this study. Effects of glucosamine-chondroitin
sulfate on glucose homeostasis may in theory be cumulative rather than immediate, so further studies that examine the type
and importance of drug-associated effects following long-term administration are warranted.
Finally, although only hypothetical, chondroprotective agents such as glucosamine may have additional adverse effects that
are unrelated to alterations in serum glucose concentration or homeostasis. This is a concern because glycosaminoglycans (such
as heparin) are known substrates in or modulators of a number of unrelated metabolic processes. In fact, prolongation of several
coagulation parameters two hours after parenteral administration of polysulfated glycosaminoglycans has been reported in dogs,3 although a later study failed to detect alterations in PT, APTT, or BMBT.1 Practitioners should keep in mind that this class of drugs has the potential for a wide range of adverse effects, particularly
those agents classified as supplements, which may not have undergone rigorous toxicity studies.
The information in "Research Updates" was provided by Erika Meler, DVM, MS, and Barrak Pressler, DVM, PhD, DACVIM, Department
of Veterinary Clinical Sciences, School of Veterinary Medicine, Purdue University, West Lafayette, IN 47907.
1. Beale BS, Goring RL, Clemmons RM, et al. The effects of semi-synthetic polysulfated glycosaminoglycan on the hemostatic mechanism
in the dog [abstr]. Vet Surg 1990;19:57.
2. McNamara PS, Barr SC, Erb HN. Hematologic, hemostatic, and biochemical effects in dogs receiving an oral chondroprotective
agent for thirty days. Am J Vet Res 1996;57(9):1390-1394.
3. Scroggie DA, Albright A, Harris MD. The effect of glucosamine-chondroitin supplementation on glycosylated hemoglobin levels
in patients with type 2 diabetes mellitus: a placebo-controlled, double-blinded, randomized clinical trial. Arch Intern Med 2003;163(13):1587-1590.