Supresión de Lesión en Células de Hígado Inducida por Dieta Alta en Grasas con Ejercicio de NataciónMohammad A. Dallak DALLAK, M. A. Suppression of high fat diet-induced liver cell injury by swim exercise. Int. J. Morphol., 36(1):327-332, 2017.
SUMMARY:The rapid rise in obesity, particularly among children is a major public health concern that adversely affects vital organs including the liver. We sought to investigate the effect of exercise on the healing of liver cells from damage induced by high fat diet (HFD) in a rat model of hepatic steatosis. Rats were randomly divided into four groups (n=6 in each group); control group fed on a low fat diet (LFD), LFD plus exercise group (LFD+EX), model group fed on HFD, and swim exercise treated group (HFD+EX). Training swim exercise started from the 11th week up until the end of week 15. Liver index and body mass index (BMI) were determined, and harvested liver tissues were examined using basic histological staining and visualised under light microscopy. In addition, collected blood samples were assayed for biomarkers of liver injury. Histological images from the model group showed accumulation of lipid droplets in the hepatocytes (steatosis) and damaged liver cells that were inhibited by swimming exercise. Compared to control groups, HFD caused an increase in BMI and liver weight but not in liver index. In addition, HFD significantly (p<0.05) increased liver injury biomarkers; high-sensitivity C-reactive protein (hsCRP) and alkaline phosphatase (ALP) that were effectively (p<0.05) decreased by swimming exercise. Furthermore, a negative correlation between these biomarkers and the antioxidant and anti-inflammatory protein adiponectin was observed. Thus, HFD-induced hepatic steatosis is treated by swim exercise.KEY WORDS: Hepatic steatosis; Swim exercise; Liver injury; Animal model.
INTRODUCTIONAbdominal obesity is a criteria of the insulin resistance syndrome, also called metabolic syndrome characterised by insulin resistance, inflammation, oxidative stress, hypertension and dyslipidaemia which carries increased risk of type-2 diabetes, cardiovascular disease, nonalcoholic fatty liver disease and cancer (Kopelman, 2000;Eckel et al., 2005;Grattagliano et al., 2008). Hepatic steatosis is the hepatic component of metabolic syndrome characterised by accumulation of fat caused by dysfunction of fat metabolism in the liver (Benlhabib et al., 2004), which is histologically comparable to liver disease caused by alcohol consumption (Sakhuja, 2014). This can lead to, if not treated, more serious complications such as nonalcoholic steatohepatitis (NASH), fibrosis, cirrhosis, liver failure and even hepatocellular carcinoma (Choi & Diehl, 2005;Paschos & Paletas, 2009). The majority of people with NASH and one-third of subjects with hepatic steatosis have high insulin resistance and low levels of adiponectin (Hui et al., 2004).Adiponectin, C-reactive protein (CRP) and ALP are known to be involved in the pathology of different types of liver injuries including non-alcoholic fatty liv...