Subchronic exposure to acrylamide leads to pancreatic islet remodeling determined by alpha cell expansion and beta cell mass reduction in adult rats.

Acrylamide (AA) is a toxic substance, used to synthesize polymers for industrial and laboratory processes. Also, AA is a food contaminant formed during the high temperature preparation of carbohydrate-rich food. The main subject of this study was to examine effects of subchronic AA treatment on the islets of Langerhans of adult rats. Adult male Wistar rats were orally treated with 25 or 50 mg/kg bw of AA for 3 weeks. Qualitative and quantitative immunohistochemical evaluation of glucagon and insulin expression and stereological analyses of pancreatic alpha and beta cells were performed. Serum insulin and glucose levels were measured. Analysis of glucagon-immunostained sections revealed a dose-dependent increase of intensity of glucagon immunopositive signal, alpha cell surface and numerical densities, volume density of alpha cell nuclei and nucleocytoplasmic ratio in AA-treated groups compared to the control. In insulin-immunolabeled pancreatic sections in AA-treated animals was observed decrease of intensity of insulin immunopositive signal, beta cell surface, numerical and volume densities and volume density of beta cell cytoplasm. Serum insulin and glucose concentrations remained unchanged after both AA treatments. The number of islets of Langerhans was not affected by AA treatment. Our results suggest that AA subchronic treatment of adult rats leads to remodeling of islet of Langerhans characterized by alpha cell expansion and beta cell mass reduction.