Where is fructose converted to glucose

How fructose disrupts the metabolism

The fructose, euphemistically also referred to as "the sweetness from fruits", has a good reputation among consumers. In nature, the simple sugar occurs mainly in fruit and vegetables. In the meantime, however, it is also added in the form of a concentrated fructose corn syrup (high fructose corn syrup, HFCS) to all kinds of processed foods, especially sweet drinks, finished products and sweets. In recent years, the fructose-glucose mixture has increasingly replaced the household sugar sucrose, which as a disaccharide also consists of half fructose and half glucose, as a sweetener in the food industry. The reason is that fructose has a higher sweetening power and can also be easily and inexpensively made from corn starch.

This added sugar appears to be fueling the obesity wave. Germans consume an average of 60 to 80 g of free sugar per day. That's more than twice what the World Health Organization recommends. Nutrition biologist Dr. Kimber L. Stanhope in a review article in the journal "Critical Reviews in Clinical Laboratory Sciences" (2016, DOI: 10.3109 / 10408363.2015.1084990).

According to this, epidemiological data show a connection between added sugar and the development of obesity, fatty liver disease, lipid metabolism disorders, insulin resistance, type 2 diabetes, cardiovascular diseases, metabolic syndrome and elevated uric acid levels.

Since metabolic and heart diseases are closely related to obesity, sugar consumption is most likely indirectly harmful - i.e. through an increase in body weight. In addition, there is also evidence of direct damage. It is based on the following physiological mechanism: The uptake of fructose in the liver is not regulated, unlike in the case of glucose, so that an excess can occur in the liver with increased consumption. Fructose cannot be stored and is therefore converted into fat.

The new synthesis of fatty acids (de novo lipogenesis) increases the fatty acid level in the liver, which means that the breakdown of fatty acids (β-oxidation) is inhibited. Overall, this leads to fatty liver disease, an increase in blood lipid values ​​and the formation and secretion of VLDL1 (very low density lipoprotein 1). In addition, increased liver lipids seem to cause insulin resistance, which in turn increases de novo lipogenesis. A vicious circle arises.

In clinical studies carried out by Stanhope's working group, the consumption of fructose-sweetened beverages over a period of ten weeks in overweight subjects increased de novo lipogenesis, blood lipid levels and uric acid concentration in the blood and decreased insulin sensitivity and β-oxidation . Glucose-sweetened drinks did not have these negative consequences in the same test subjects.

Increased risk of gout

According to the review, the fructose excess sets a further mechanism in motion in the liver: Since the fructose is metabolized with ATP consumption, a phosphate depletion and an AMP excess occurs. This activates the enzyme AMP deaminase, which first breaks down AMP into inosine monophosphate and then further into uric acid. A high fructose consumption can lead to hyperuricemia and thus to gout (read also gout: fructose possible triggers).