NAFLD (non-alcoholic fatty liver disease) currently affects 25% of the human population, with its prevalence on the rise. At least a quarter of this population will evolve from simple steatosis to NASH (steatohepatitis), increasing the risk of liver fibrosis and cirrhosis. Liver steatosis or fatty liver is reversible and involves the accumulation of TG (triglycerides) in the form of lipid droplets in at least 5% of the hepatocytes.
NAFLD, either in the form of fatty liver or NASH/cirrhosis, is a risk factor for hepatocellular carcinoma. Although fatty liver can be theoretically prevented or treated effectively by changes in lifestyle through addressing dietary habits and physical activity, these changes are difficult to maintain over time.
Unfortunately, there is no approved drug therapy for NAFLD, and there is an urgent need to fill this void therapeutic niche.
A high-fat diet is not enough to cause short-term fatty liver disease. However, if this diet is combined with the intake of beverages sweetened with liquid fructose, the accumulation of fats in the liver accelerates and hypertriglyceridemia —a cardiovascular risk factor— can appear.
Fructose is one of the most common sweeteners in the food industry. This simple sugar (monosaccharide) is industrially obtained from corn syrup, a product derived from this gramineae. With a great sweetener power and low production costs, fructose is used by the food industry to sweeten beverages, sauces and processed foods, despite the scientific evidence that associates it with metabolic diseases which are risk factors of cardiovascular pathologies.
According to the 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 particular, fructose intake affects directly the expression and activity of the nuclear factor ChREBP. Once activated, this factor causes an increase in the expression of enzymes that control the hepatic synthesis of fatty acids", he continues. "Parallelly, fructose intake reduces the activity of the nuclear receptor PPARalfa, which is the main responsible for the controlling of the expression of genes that code the enzymes involved in the fatty acid oxidation (mitochondrial and peroxisome) in the liver.
However, when we eat fruit, the amount of taken fructose is a lot lower compared to a sweetened drink. Also, the process of chewing it and the presence of other elements in the fruit, such as fiber, slows down the absorption of fructose and its arrival to the liver.
NAFLD, either in the form of fatty liver or NASH/cirrhosis, is a risk factor for hepatocellular carcinoma. Although fatty liver can be theoretically prevented or treated effectively by changes in lifestyle through addressing dietary habits and physical activity, these changes are difficult to maintain over time.
Unfortunately, there is no approved drug therapy for NAFLD, and there is an urgent need to fill this void therapeutic niche.
A high-fat diet is not enough to cause short-term fatty liver disease. However, if this diet is combined with the intake of beverages sweetened with liquid fructose, the accumulation of fats in the liver accelerates and hypertriglyceridemia —a cardiovascular risk factor— can appear.
Fructose is one of the most common sweeteners in the food industry. This simple sugar (monosaccharide) is industrially obtained from corn syrup, a product derived from this gramineae. With a great sweetener power and low production costs, fructose is used by the food industry to sweeten beverages, sauces and processed foods, despite the scientific evidence that associates it with metabolic diseases which are risk factors of cardiovascular pathologies.
According to the 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 particular, fructose intake affects directly the expression and activity of the nuclear factor ChREBP. Once activated, this factor causes an increase in the expression of enzymes that control the hepatic synthesis of fatty acids", he continues. "Parallelly, fructose intake reduces the activity of the nuclear receptor PPARalfa, which is the main responsible for the controlling of the expression of genes that code the enzymes involved in the fatty acid oxidation (mitochondrial and peroxisome) in the liver.
However, when we eat fruit, the amount of taken fructose is a lot lower compared to a sweetened drink. Also, the process of chewing it and the presence of other elements in the fruit, such as fiber, slows down the absorption of fructose and its arrival to the liver.
TFS, brother 
