Basal and Glucagon‐Stimulated Plasma C‐PeDtide Concentrations in Healthy Dogs, Dogs With Diabetes Millitus, and Dogs With Hyperadrenocorticism
Authors: Montgomery Tracey M. , Nelson Richard W. , Feldman Edward C. , Robertson Kimberly , Polonsky Kenneth S. 
Published: March 2010

Serum glucose and plasma C‐peptide response to IV glucagon administration was evaluated in 24 healthy dogs, 12 dogs with untreated diabetes mellitus, 30 dogs with insulin‐treated diabetes mellitus, and 8 dogs with naturally acquired hyperadrenocorticism. Serum insulin response also was evaluated in all dogs, except 20 insulin‐treated diabetic dogs. Blood samples for serum glucose, serum insulin, and plasma C‐peptide determinations were collected immediately before and 5,10,20,30, and (for healthy dogs) 60 minutes after IV administration of 1 mg glucagon per dog. In healthy dogs, the patterns of glucagon‐stimulated changes in plasma C‐peptide and serum insulin concentrations were identical, with single peaks in plasma C‐peptide and serum insulin concentrations observed approximately 15 minutes after IV glucagon administration. Mean plasma C‐peptide and serum insulin concentrations in untreated diabetic dogs, and mean plasma C‐peptide concentration in insulin‐treated diabetic dogs did not increase significantly after IV glucagon administration. The validity of serum insulin concentration results was questionable in 10 insulin‐treated diabetic dogs, possibly because of anti‐insulin antibody interference with the insulin radioimmunoassay. Plasma C‐peptide and serum insulin concentrations were significantly increased (P <.001) at all blood sarnplkg times after glucagon administration in dogs with hyperadrenocorticism, compared with healthy dogs, and untreated and insulin‐treated diabetic dogs. Five‐minute C‐peptide increment, C‐peptide peak response, total C‐peptide secretion, and, for untreated diabetic dogs, insulin peak response and total insulin secretion were significantly lower (P <.001) in diabetic dogs, compared with healthy dogs, whereas these same parameters were significantly increased (P < .011 in dogs with hyperadrenocorticism, compared with healthy dogs, and untreated and insulin‐treated diabetic dogs. Although not statistically significant, there was a trend for higher plasma C‐peptide concentrations in untreated diabetic dogs compared with insulin‐treated diabetic dogs during the glucagon stimulation test. Baseline C‐peptide concentrations also were significantly higher (P <.05) in diabetic dogs treated with insulin for less than 6 months, compared with diabetic dogs treated for longer than 1 year. Finally, 7 of 42 diabetic dogs had baseline plasma C‐peptide concentrations greater than 2 SD (ie, >0.29 pmol/mL) above the normal mean plasma C‐peptide concentration; values that were significantly higher, compared with results in healthy dogs (P < .001) and with the other 35 diabetic dogs (P < .001). In summary, measurement of plasma C‐peptide concentration during glucagon stimulation testing allowed differentiation among healthy dogs, dogs with impaired β‐cell function (ie, diabetes mellitusl, and dogs with increased β‐cell responsiveness to glucagon (ie, insulin resistance). Plasma C‐peptide concentrations during glucagon stimulation testing were variable in diabetic dogs and may represent dogs with type‐1 and type‐2 diabetes or, more likely, differences in severity of β‐cellloss in dogs with type‐1 diabetes.J Vet Intern Med 1996;10:116–122. Copyright ©1996by the American College of Veterinary Internal Medicine.