ESPE Abstracts

Introduction & Objectives: High consumption of processed foods rich in fat and sugar are associated with the increasing prevalence of metabolic disturbances like obesity, insülin resistance, dyslipidemia, type 2 diabetes mellitus. In the present study, we aimed to investigate the relationship between advanced glycation end products and metabolic disorders such as insulin resistance caused by high fructose and high-fat diet, and also examine histological changes in the pancreas, in a rat model.

Materials & Methods: Twenty-four Sprague Dawley ratswere randomly divided into three groups (8 rats per group) as control, high fructose and high-fat groups. The rats of control group were given with normal rat control diet. In the high fructose group; the rats were fed with %60 high fructose diet andin the high fatty group, the rats were given %45 high fat diet. After 12 weeks, rats in all groups were euthanized under anesthesia. Blood samples for biochemical analysis and tissue samples for histological investigation were taken. Tissue sections were stained with immunohistochemical staining for detection of AGE and R-AGE expression.

Results: Biochemical results were given in Table. In the pancreas of rats fed with high fructose diet and high-fat diet, the normal histological structure was observed to be impaired both in the exocrine and endocrine sections.

Rats fed with high fructose feed had intracellular swelling and vacuolization in islet cells and edema was seen in intercellular areas. In rats fed with fatty diet, interstitial edema, swelling of cells and intracytoplasmic vacuoles were observed in the Langerhans islets and the nuclei of some cells were lost. AGE and R-AGE immunopositivity both in the high fructose and high-fat groups were increased when compared with the control group.

Conclusion: Our results showed that high fructose and high-fat diet lead to both exocrine and endocrine pancreas injury, and this damage may be related to high expression of AGE and R-AGE.