Physiology and histopathology of pancreas in canine diabetes mellitus: Review

Abstract

Canine Diabetes Mellitus (CDM) is represented as a group of autoimmune metabolic diseases of multifactorial etiology. In CDM there is a relative or absolute deficiency of insulin that leads to a failure of the cells to obtain and use glucose. Are most cases, diagnosed dogs will be insulin dependent for all life, and when the disease is not treated will the consequence is death. The objective of this review was to study the histopathology and physiology of the pancreas to understand the etiopathogenesis of CDM, based on the description of pancreatic pathological changes resulting from it or that favor its occurrence. The methodology of this research was to review literature from books and scientific production in veterinary medicine, based on research related to the following. Currently, there is no internationally defined criterion for the classification of diabetes in small animal. Classification of CDM according to the human model is common, bit some authors defend the use of primary and secondary CDM. The main histological alterations of the pancreas in dog with CDM include partial or total destruction of the islets of Langerhans, vacuolization and/or hydropic degeneration, presence of leukocyte infiltration, although divergent between authors, and antibodies when immune-mediated; amyloid deposits are also described, predisposing to glucotoxity. Some pancreatic changes are caused by CDM as a consequence, but the opposite also occurs. The autoimmune physiological mechanisms together with genetic and environmental factors, insulin antagonist drugs and adjacent diseases play an important role in the development and progression of CDM, resulting in the irreversible loss of function of β-pancreatic cells.