Background:
Over the past 40 years one of the most widely used industrial sweeteners in processed foods and beverages is fructose. Consumption of a high-fructose diet (HFD) is tightly associated with an increasing frequency of multiple disorders including visceral obesity and cardiovascular diseases (CVDs). The latter are considered the leading cause of death globally. Since the consequences HFD consumption in animals have similar effects to those seen in humans, animal models of obesity are widely used for research purposes. The aim of this study was to investigate the pathogenic link between a.abdominalis wall changes and fructose-induced obesity in rats.

Material and Methods:
We used a rat model of HFD (HFD-12 weeks, 20 % glucose-fructose corn syrup). Male Wistar rats were assigned to two experimental groups (n=8): control and HFD group. Over the whole experimental period, all animals were provided with a standard rodent diet and tap water ad libitum. Zoometric measurements, body mass index (BMI) and morphometric parameters of the abdominal aorta were analyzed. Routine histological and immunohistochemical staining techniques (SOD-1, NOS3 - oxidative stress and endothelial dysfunction markers- FLT-1) were applied to evaluate the pathomorphological changes in aortic wall using Aperio Image Scope software. The functional properties of the abdominal aorta were assessed through the Kernogan’s index (KI) calculation.

Results:
Оur results demonstrate higher values of BMI, aortic wall thickness and Kernogan’s index in HFD group compared to the controls. Furthermore, immunohistochemical endothelial expression of SOD-1 in the HFD group was increased whereas NOS3 and FLT-1 - reduced.

Conclusions:
HFD causes visceral obesity, increased BMI, oxidative stress and pathomorphological and dysfunctional changes in the aortic wall that may be associated with the development of endothelial dysfunction and CVDs.