2016 ACVIM Forum Research Abstract Program

HOMEOSTASIS DETERIORATES MORE RAPIDLY WITH AGE IN BURMESE CATS COMPARED TO NON-BURMESE. Margareth Rose Lederer 1 , Jacquie Rand 2 , Nubia Lopes 2 , John Morton 3 , Nick Jonsson 1 . 1 University of Glasgow, Glasgow, Scotland, UK, 2 University of Queensland, Gatton, Qld, Australia, 3 Jemora Pty Ltd., Geelong, Vic., Australia Burmese cats are predisposed to diabetes mellitus in Australia, New Zealand and United Kingdom, and the disease is 3 to 4 times more prevalent in this breed compared to domestic cats. Mechanisms predisposing Burmese cats to diabetes remain unclear. This study compared hormonal and biochemical variables associated with glucose and lipid metabolism between mixed-age, lean to overweight, clinically healthy Burmese and non-Burmese cats. Burmese cats older than 3.5 years had higher fasting glucose compared to non-Burmese (P = 0.02), with 1.3 mmol/L higher at 3.5 years and 3.5 mmol/L higher at 10 years of age (P < 0.001), but not at 2 years of age. Mean and 2-hr glucose concentrations during a glucose tolerance test were higher in Burmese than non-Burmese cats (P < 0.006 to 0.031), indicating relative glucose intolerance. Lean Burmese cats had 4.8 lU/mL higher fasting insulin concentrations than non-Burmese, suggesting they are insulin resistant (P = 0.031). At time 10 minutes during the GTT, Burmese cats had lower insulin concentration compared to non-Burmese, but were higher at 120 minutes (P = 0.066 and P = 0.046). This is consistent with diminished first phase, and increased and prolonged second phase insulin release, a pattern of insulin secretion described in prediabetic, diabetic, obese humans and obese cats. Fasting triglyceride concentration was 0.2 mmol/L higher (P = 0.015) and fasting NEFA concentration was 0.18 mmol/L higher (P = 0.016) in Burmese compared to non-Burmese. These results demonstrate that Burmese cats have more rapid deterioration of b-cell function with age, and impaired glucose homeostasis and lipid metabolism occur concurrently in these cats. Previous studies indicated that serum fructosamine level is decreased in hyperthyroid cats; however, its clinical utility in diabetic hyperthyroid cats was not reported. We hypothesized that hyperthyroidism in diabetic cats will result in a clinically significant decrease in serum fructosamine level compared to euthyroid diabetic cats. Data of serum total thyroxine (TT4) and fructosamine of hyperthyroid/euthyroid diabetic/nondiabetic cats from the New Zealand Veterinary Pathology and Colorado State University were retrieved and statistically analyzed. Serum fructosamine was significantly lower in hyperthyroid diabetic than euthyroid diabetic cats (mean 332 µmol/L 95% CI 291-379, n = 18 versus mean 527 µmol/L 95% CI 515-553, n = 186) while not different between hyperthyroid diabetic and euthyroid nondiabetic cats (mean 332 µmol/L 95% CI 291-379, n = 18 versus mean 321 µmol/L 95% CI 296-345, n = 128). There was a significant negative correlation between serum TT4 concentration and serum fructosamine and glucose concentrations (n = 659, P < 0.01, and n = 297, P < 0.01, respectively). Hyperthyroid cats (diabetic or not) had significantly (P < 0.05) lower serum glucose than euthyroid cats (diabetic or not). Diabetes and random variability accounted for 49.7% and 45.4% of the change in serum fructosamine; whereas, age (3.1%) and population (1.8%) had minimal impact on serum fructosamine. In conclusion, in the current study, serum fructosamine concentration was si