Swim exercise training ameliorates hepatocyte ultrastructural alterations in rats fed on a high fat and sugar diet

Mohammed A Dallak, Ismaeel Bin-Jaliah, Alia Albawardi, Mohamed A Haidara, Hussein F Sakr, Refaat A Eid, W N Hassan, Bahjat Al-Ani
Ultrastructural Pathology 2018, 42 (2): 155-161
Excessive consumption of carbohydrate and fat increases the risk of liver disease. We hypothesized that swim exercise can protect hepatocytes from ultra-structural damage induced by high cholesterol and fructose diets (HCFD). Rats were either fed with HCFD (model group) or a standard laboratory chow (control group) for 15 weeks before being sacrificed. Swim exercise trained rats started the treatment from the 11th week until the sacrifice day, end of week 15. Blood samples were assayed for biomarkers of liver injury and adiponectin. The harvested liver tissues were examined using transmission electron microscopy (TEM). TEM images revealed substantial damage and accumulation of lipid droplets (steatosis) in the hepatocytes of the model group that was inhibited by swim exercise. In addition, HCFD significantly (p < 0.0005) increased insulin resistance index (HOMA-IR), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), alanine aminotransferase (ALT), and aspartate aminotransferase (AST), which were effectively (p < 0.02) decreased by a swim exercise to levels comparable to control group. Whereas, swim exercise increased adiponectin levels in HCFD group (p < 0.03). These results show that HCFD-induced hepatic injury is ameliorated by swim training exercise possibly via restoration of a normal blood sugar and lipid, induction of adiponectin and inhibition of inflammatory, and liver injury biomarkers.

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