A high-fat diet isn''t enough to cure short-term fatty liver illness. However, when combined with the use of liquid fructose, the accumulation of fats in the liver accelerates and hypertriglyceridemia a cardiovascular risk factor can arise.
This is revealed in a study on a mouse experiment conducted in the journalMolecular Nutrition and Food Research, led by Professor Juan Carlos Laguna from the University of Barcelona''s Biomedicine Institute (IBUB) and the Physiopathology of Obesity and Nutrition Networking Biomedical Research Centre (CIBEROBN).
Among other researchers, Aleix Sala-Vila and Iolanda Lazaro, researchers at the Hospital del Mar Medical Research Institute (IMIM), and Jose Rodriguez-Morato, researchers at the IMIM-Hospital del Mar and MELIS-Pompeu Fabra University.
Fructose and lipid metabolism
Despite scientific evidence that fructose is associated with metabolic diseases, this simple sugar (monosaccharide) is industrially obtained from corn syrup, a product derived from this gramineae. Despite its excellent sweetener power and reduced production costs, fructose is used by the food industry to sweeten beverages, sauces, and processed foods.
According to a new study, the effect caused by fructose in the increase in the synthesis of fatty acids in the liver is more decisive than the external introduction of fats through the diet. In high-fat foods, this monosaccharide is able to induce an increase in the de novo lipogenesis, namely, the formation of fats through sugar and an inhibition of the lipid oxidation in the liver.
In addition, fructose intake influences directly the expression and activity of the nuclear factor ChREBP. Once activated, this factor continues the expression of enzymes that control the hepatic synthesis of fat acids. Parallelly, fructose intake reduces the activity of the nuclear receptor PPARalfa, which is the primary component responsible for controlling the expression of genes involved in the fatty acid oxidation (mitochondrial and peroxisome) in the liver.
The combination of saturated fat from dietary origin and the induction of the endogen synthesis of fatty acids is to make the liver appear, according to Nuria Roglans, the author of the study and member of the mentioned Department.
Fatty liver disease in humans
Several epidemiologic studies related the consumption of beverages that are sweetened with fructose to the non-alcoholic fatty liver disease (NAFLD), a pathology for which no specific pharmacological therapy exists. De novo lipogenesis in these patients increases to a 30% of the lipids accumulated in the liver, while in healthy individuals, this synthesis reduces the concentration of his hepatic lipids.
The animal model developed by the team will be of great interest to develop future therapeutics to treat the non-alcoholic fatty liver disease (NAFLD). People with this pathology have a greater endogenous synthesis of lipids in the liver than healthy individuals. Therefore, the effects described in this study may appear in humans as well, according to experts.
Unfortunately, the fatty liver is the beginning point for more serious pathologies, such as steatohepatitis and cirrhosis. It is a practically asymptomatic pathology, although some mild unspecific digestive problems may arise. For the time being, there is no effective treatment for this pathology.
When fructose is administered in its liquid form, it is rapidly absorbed and it touches the liver massively, resulting in the described metabolic alterations. To obtain a comparison, the team may look at the appearance of a fructose overdose when it is taken in sweetened beverages.
However, when we eat fruit, the amount of taken fructose is significantly lower than in a sweetened beverage. Besides, the process of chewing it and the presence of other components in the fruit, such as fiber, hinder the absorption of fructose and its delivery to the liver, according to the authors.