Morphological and Biochemical Investigation of the Healing Effects of Exercise on High Fat Diet Induced Kidney and Bladder Damage

Objective: The aim of this study was to evaluate the ameliorative effects of swimming training on renal and bladder damage caused by a highfat diet (HFD) using morphological and biochemical measurements. Methods: Sprague Dawley rats were fed either standard chow (CONT, 6% fat) or HFD (45% fat) for 18 weeks, these rats were divided into two subgroups at the last 6 weeks of the experiment. The exercise groups (CONT+EXC, HFD+EXC) were trained daily swimming sessions (1 h per day for 5 days/week) during the last 6 weeks. Kidney and bladder samples were prepared for light and electron microscopic examination at the end of experiment. Malondialdehyde, glutathione, interleukin-6, and tumor necrosis factor-a were measured by biochemically. Results: Regular morphology of the renal cortex and bladder mucosa was observed in the CONT and CONT +EXC groups. Degenerated renal corpuscles and proximal tubules in the kidney and degenerated urothelium with leaky tight junctions and mast cell increase in the bladder mucosa were observed in the HFD group. Ameliorated renal cortex and bladder mucosa were observed in the HFD+EXC group. In addition, malondialdehyde, glutathione, interleukin-6, and tumor necrosis factor-a levels were also consistent with the histological findings. Conclusion: HFD-induced renal and bladder damage may be related to increased oxidative damage. It was observed that the histological damage and altered oxidative stress parameters could be reversed by swimming training, and it is thought that moderate swimming exercise may play a role in regulating oxidative stress.

Automated summary

The aim of this study was to evaluate the ameliorative effects of swimming training on renal and bladder damage caused by a high-fat diet. The results showed that swimming training could reverse the histological damage and altered oxidative stress parameters, suggesting its potential role in regulating oxidative stress.