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.