Fructose in the Diet Leads to Fatty Liver & Promotes Metabolic Disease

The amount of fructose in the typical American diet has increased dramatically in the past 20 years. This is due primarily to the increased use of high fructose corn syrup (HFCS) as a sweetener is processed foods and drinks, especially soft drinks. The use of HFCS as a sweetener stems from the fact that the US grows significantly more corn than sugar beets or cane sugar and it is relatively easy and inexpensive to chemically convert some of the glucose in corn starch (starch being a polymer of glucose) to fructose. Consumption of soft drinks (high in HFCS) is associated with an increased risk for obesity in adolescents and for development of type 2 diabetes in young and middle-aged women. Excess fruit juice (also rich in fructose) is also associated with the development of obesity in children. One cannot, however, assume that the culprit is exclusively HFCS. In the typical Western-style diet there is an overall excess of caloric intake that contribute to obesity, diabetes, heart disease, and numerous other ailments. However, this is not to say that fructose is an “innocent” molecule. Indeed, consumption of fructose has been shown to be highly correlated with the development of diabetes, fatty liver diseases, obesity and the metabolic syndrome. Consumption of soft drinks (high in HFCS) is associated with an increased risk for obesity in adolescents and for type 2 diabetes in young and middle-aged women. Excess fruit juice (also rich in fructose) is also associated with the development of obesity in children. These effects are related to the mechanism of fructose metabolism versus that of glucose and also to the effects of fructose metabolism in the brain on appetite and feeding behaviors. For the details go to the Fructose Metabolism page of themedicalbiochemistrypage.org

New data recently e-published in the American Journal of Clinical Nutrition demonstrates that dietary fructose, even under conditions of normal caloric intake, leads to hepatic damage and endotoxemia contributing to the development of hepatic steatosis (fatty liver) and non-alcoholic fatty liver disease (NAFLD). This is significant because hepatic steatosis is highly correlated with diabetes and cardiovascular disease.


This research is significant to human health for a number of reasons, the most importnat being that the data was acquired with the use of primates and not mice which are the more commonly used mammalian model. The other significant fact is that the damaging effects of fructose were observed even when the animals were fed a normal caloric diet.

The experiments performed in this published study demonstrated that high dietary fructose consumption rapidly induces liver fatty infiltration, inflammation, and damage. Significantly, these hepatic changes were shown to occur in a short time period and under conditions when the caloric intake was controlled and there were no changes in the gut microbiome, overall levels of adiposity, or development of signs of the metabolic syndrome.


The take-home from these studies is that even if one carefully watches the total calories consumed in order to maintain a normal body mass index (i.e. low total adiposity), if too many of the calories are delivered in the form of fructose, either as HFCS or sucrose (a disaccharide of glucose and fructose) metabolic disruption and disease can result.

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