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- Author or Editor: Lawren L. Durocher x
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Abstract
Objective—To examine acid-base and hormonal abnormalities in dogs with diabetes mellitus.
Design—Cross-sectional study.
Animals—48 dogs with diabetes mellitus and 17 healthy dogs.
Procedures—Blood was collected and serum ketone, glucose, lactate, electrolytes, insulin, glucagon, cortisol, epinephrine, norepinephrine, nonesterified fatty acid, and triglyceride concentrations were measured. Indicators of acid-base status were calculated and compared between groups.
Results—Serum ketone and glucose concentrations were significantly higher in diabetic than in healthy dogs, but there was no difference in venous blood pH or base excess between groups. Anion gap and strong ion difference were significantly higher and strong ion gap and serum bicarbonate concentration were significantly lower in the diabetic dogs. There were significant linear relationships between measures of acid-base status and serum ketone concentration, but not between measures of acid-base status and serum lactate concentration. Serum insulin concentration did not differ significantly between groups, but diabetic dogs had a wider range of values. All diabetic dogs with a serum ketone concentration > 1,000 μmol/L had a serum insulin concentration < 5 μU/mL. There were strong relationships between serum ketone concentration and serum glucagon-insulin ratio, serum cortisol concentration, and plasma norepinephrine concentration. Serum β-hydroxybutyrate concentration, expressed as a percentage of serum ketone concentration, decreased as serum ketone concentration increased.
Conclusions and Clinical Relevance—Results suggested that ketosis in diabetic dogs was related to the glucagon-insulin ratio with only low concentrations of insulin required to prevent ketosis. Acidosis in ketotic dogs was attributable largely to high serum ketone concentrations.
Abstract
Objective—To determine whether prolonged exercise by conditioned sled dogs affects urine concentrations of homovanillic acid (a metabolite of dopamine), vanillylmandelic acid (a metabolite of norepinephrine and epinephrine), and cortisol.
Animals—24 conditioned Alaskan sled dogs (2 to 8.5 years old) that were in training for a multiday endurance race.
Procedures—Voided urine samples were collected from 4 groups of dogs (randomly selected from 54 dogs) after no exercise (control group; n = 6 dogs), completion of a 160km run (group A; 3), completion of a 420-km run (group B; 7), and completion of a 560-km run (group C; 6). Urine cortisol concentrations were determined by use of an immunoassay technique; urine vanillylmandelic acid and homovanillic acid concentrations were measured via high-performance liquid chromatography.
Results—Compared with the control group, urine cortisol concentration in groups A, B, and C was significantly different (5.33 × 10−4 ± 2.62 × 10−4 μg/dL vs 1.04 × 10−4 ± 2.31 × 10−5 μg/dL, 8.88 × 10−4 ± 5.49 × 10−4 μg/dL, and 6.31 × 10−4 ± 5.09 × 10−4 μg/dL, respectively). Urine homovanillic acid concentration did not differ among the 4 groups. Vanillylmandelic acid was not detected in any urine samples.
Conclusions and Clinical Relevance—Results indicated that prolonged exercise by sled dogs did not affect urine homovanillic acid concentration but did increase urinary cortisol secretion, which is indicative of adrenocortical stimulation. The apparent lack of vanillylmandelic acid in voided urine samples requires further investigation.
