4.3.2 The risk of fatty liver disease in the offspring
It has been previously shown that excessive fructose consumption leads to dysfunctions in various tissues and organs, including liver, adipose tissue, pancreatic, skeletal muscle, kidney, heart, brain, and intestine (Muriel et al.,2021). The primary metabolites of fructose metabolism are produced in the liver and secreted into the circulation, directly affecting tissue and organ functions (Zhang et al., 2019). In humans, 70% of fructose is metabolized in the liver, so a high fructose diet induces hepatic - fatty acid synthesis and triglyceride accumulation (Muriel et al., 2021). Since uncontrolled lipid metabolism is associate with the development of non-alcoholic fatty liver disease (NASH) hepatic steatosis was studied in the offspring. It is a term widely used to describe excessive fatty infiltration in the liver in the absence of alcohol, autoimmune disorders, or viral hepatitis; it is attributed to obesity, high sugar and fat consumption, and sedentarism (Horst and Serlie, 2017). The current study observed that maternal fructose consumption during pregnancy leads to an increased area of steatosis in the livers of male and female offspring, compared to the water groups.
Furthermore, it is suggested that physical exercise is capable of decreasing intrahepatic lipids and the formation of lipid droplets, decreasing free fatty acids and the effects of lipotoxicity, since increased levels of free fatty acids can be toxic to the body cells, and their sequestration by lipid droplets provides a buffering capacity that prevents lipotoxicity (Olzmann & Carvalho, 2019). Indeed in our current study, the maternal physical exercise interventions were able to reduce hepatic steatosis, demonstrating that the practice of voluntary physical exercise by the mothers has a hepatic protective effect in the offspring.