Research Communications of the 27(th) ECVIM-CA Congress: Intercontinental, Saint Julian's, Malta, 14th to 16th September 2017

Disclosures: No disclosures to report. Dysfunctional pancreatic beta-cells are crucial in the pathophysiology of diabetes. Based on light microscopy, diabetic cats have reduced number of beta-cells but whether secretory granules and mitochondria, which are central to cellular function and viability, have abnormal morphology is unknown. Furthermore, a recent investigation questioned the role of islet amyloid in the pathogenesis of diabetes in cats since its amount did not differ between diabetic and age-matched control cats. However, intracellular aggregation of amylin into oligomers, rather than extracellular amyloid, may be the principle of beta-cell toxicity in type 2 diabetes. Therefore, the aims of the study were to characterize ultrastructural lesions of beta-cells in diabetic cats with emphasis on granules, mitochondria and intracellular amylin aggregation. Pancreases of diabetic and control cats euthanized for any disease were prospectively collected. Samples were harvested within 1 h from death and glutaraldehyde-fixed. Control cats were selected to be matched for age, sex and body weight. Sections were prepared for electron microscopy and immunogold labeling by using antiinsulin and anti-amylin antibodies. Beta-cell morphology was assessed, including beta-cell granule area, eccentricity (minimum-tomaximum diameter ratio), granule number, as well as beta-cell mitochondrial area, number and inter-cristae distance. Intracellular accumulation of amylin-positive material outside the granules was explored. Non-parametric tests were used for statistical analysis.