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Evaluation of beta-cell sensitivity to glucose and first-phase insulin secretion in obese dogs

Kurt R. Verkest BVSc1, Linda M. Fleeman BVSc, PhD2, Jacquie S. Rand BVSc, DVSc3, and John M. Morton BVSc, PhD4
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  • 1 Centre for Companion Animal Health, School of Veterinary Science, The University of Queensland, St Lucia, QLD 4072, Australia.
  • | 2 Centre for Companion Animal Health, School of Veterinary Science, The University of Queensland, St Lucia, QLD 4072, Australia.
  • | 3 Centre for Companion Animal Health, School of Veterinary Science, The University of Queensland, St Lucia, QLD 4072, Australia.
  • | 4 Centre for Companion Animal Health, School of Veterinary Science, The University of Queensland, St Lucia, QLD 4072, Australia.

Abstract

Objective—To compare beta-cell sensitivity to glucose, first-phase insulin secretion, and glucose tolerance between dogs with naturally occurring obesity of > 2 years' duration and lean dogs.

Animals—17 client-owned obese or lean dogs.

Procedures—Frequently sampled IV glucose tolerance tests were performed with minimal model analysis on 6 obese dogs and matched controls. Glucagon stimulation tests were performed on 5 obese dogs and matched controls.

Results—Obese dogs were half as sensitive to the effects of insulin as lean dogs. Plasma glucose concentrations after food withholding did not differ significantly between groups; plasma insulin concentrations were 3 to 4 times as great in obese as in lean dogs. Obese dogs had plasma insulin concentrations twice those of lean dogs after administration of glucose and 4 times as great after administration of glucagon. First-phase insulin secretion was greater in obese dogs.

Conclusions and Clinical Relevance—Obese dogs compensated for obesity-induced insulin resistance by secreting more insulin. First-phase insulin secretion and beta-cell glucose sensitivity were not lost despite years of obesity-induced insulin resistance and compensatory hyperinsulinemia. These findings help explain why dogs, unlike cats and humans, have not been documented to develop type 2 diabetes mellitus.

Abstract

Objective—To compare beta-cell sensitivity to glucose, first-phase insulin secretion, and glucose tolerance between dogs with naturally occurring obesity of > 2 years' duration and lean dogs.

Animals—17 client-owned obese or lean dogs.

Procedures—Frequently sampled IV glucose tolerance tests were performed with minimal model analysis on 6 obese dogs and matched controls. Glucagon stimulation tests were performed on 5 obese dogs and matched controls.

Results—Obese dogs were half as sensitive to the effects of insulin as lean dogs. Plasma glucose concentrations after food withholding did not differ significantly between groups; plasma insulin concentrations were 3 to 4 times as great in obese as in lean dogs. Obese dogs had plasma insulin concentrations twice those of lean dogs after administration of glucose and 4 times as great after administration of glucagon. First-phase insulin secretion was greater in obese dogs.

Conclusions and Clinical Relevance—Obese dogs compensated for obesity-induced insulin resistance by secreting more insulin. First-phase insulin secretion and beta-cell glucose sensitivity were not lost despite years of obesity-induced insulin resistance and compensatory hyperinsulinemia. These findings help explain why dogs, unlike cats and humans, have not been documented to develop type 2 diabetes mellitus.

Contributor Notes

Dr. Fleeman's present address is Animal Diabetes Australia, Boronia 3155, Australia.

Dr. Morton's present address is Jemora Pty Ltd, PO Box 2277, Geelong 3220, VIC, Australia.

Supported by Nestlé Purina PetCare.

Presented in abstract form at the American College of Veterinary Internal Medicine Forum, Baltimore, June 2005.

The authors thank Lyn Knott, Rebekah Scotney, Libby Jolly, Fiona Tremaine, and Sarah Norris for technical assistance.

Address correspondence to Dr. Verkest (k.verkest@uq.edu.au).