Unlike glucose (the simplest sugar, and the foundation of carbohydrate energy use in the body), which can be metabolized and used for energy by cells throughout the body, fructose (fruit sugar) must be metabolized through a rather complex process in the liver, where some of it becomes glucose eventually, and a substantial portion is bound in triglycerides, destined to become very-low-density lipoproteins (VLDL) or be stored as fat (or to clog arteries as VLDL cholesterol).
A new study shows that this process, fructolysis, increases uric acid levels in the liver and decreases ATP levels (the energy that powers cells) - this was with obese and diabetic subjects, but there is ample evidence that this is not confined only to this population.
For the present study, 244 obese and diabetic adults from the Look AHEAD Study were evaluated, with dietary fructose consumption estimated by the food frequency questionnaire. Liver ATP and uric acid levels were measured in 105 patients who participated in the Look AHEAD Fatty Liver Ancillary Study. Researchers assessed the change in liver ATP content using an IV fructose challenge in 25 subjects, comparing patients with low fructose consumption (less than 15 grams per day) to those with high fructose consumption (greater than 15 grams per day).The study citation, as given in the press release:
The team found that participants with a high intake of dietary fructose had lower liver ATP levels at baseline and a greater change in ATP content following the fructose challenge than those who consumed a lower amount of fructose. Patients with high uric acid levels (5.5 mg/dL or more) displayed lower ATP stores in response to fructose.
Dr. Abdelmalek concludes, “High fructose consumption and elevated levels of uric acid are associated with more severe depletion of liver ATP. Our findings suggest that increased dietary fructose intake may impair liver “energy balance.” Further research to define the clinical implications of these findings on metabolism and NAFLD is necessary.” The authors highlight the importance of public awareness of the risks associated with a diet high in fructose.
“Higher Dietary Fructose Is Associated with Impaired Hepatic ATP Homeostasis in Obese Individuals with Type 2 Diabetes.” Manal F. Abdelmalek, Mariana Lazo, Alena Horska, Susanne Bonekamp, Edward W. Lipkin, Ashok Balasubramanyam, John P. Bantle, Richard J. Johnson, Anna Mae Diehl, Jeanne M. Clark, and the Fatty Liver Subgroup of the Look AHEAD Research Group. Hepatology; (DOI: 10.1002/hep.25741); Print Issue Date: September, 2012. URL: http://onlinelibrary.wiley.com/doi/10.1002/hep.25741/abstract
Here is some additional information on fructose metabolism from Wikipedia:
MetabolismIn a 2012 meta-analysis of controlled feeding clinical trials, fructose was not an independent factor for weight gain. Fructose consumption did cause weight gain in a diet with excessive calories, which could be due to the extra calories rather than fructose per se.
Excess fructose consumption has been hypothesized to be a cause of insulin resistance, obesity, elevated LDL cholesterol and triglycerides, leading to metabolic syndrome. In preliminary research, fructose consumption was correlated with obesity. A study in mice showed that a high fructose intake may increase adiposity.
Although all simple sugars have nearly identical chemical formulae, each has distinct chemical properties. This can be illustrated with pure fructose. A journal article reports that, "...fructose given alone increased the blood glucose almost as much as a similar amount of glucose (78% of the glucose-alone area)".
In Wistar fatty rats, a laboratory model of diabetes, 10% fructose feeding as opposed to 10% glucose feeding was found to increase blood triglyceride levels by 86%, whereas the same amount of glucose had no effect on triglycerides. Neither glucose nor fructose influenced insulin or blood sugar in this model. The authors concluded "These results show that in genetically obese, diabetic rats feeding fructose and glucose is associated with an increase in hepatic lipogenic enzyme activities and triglyceride production, and suggest that fructose stimulates triglyceride production but impairs triglyceride removal, whereas glucose stimulates both of them.
Another study in humans concluded that fructose and sucrose are metabolized similarly, whereas a different analysis "produced significantly higher fasting plasma triglyceride values than did the glucose diet in men" and "...if plasma triacylglycerols are a risk factor for cardiovascular disease, then diets high in fructose may be undesirable".
Fructose is a reducing sugar, as are all monosaccharides. The spontaneous chemical reaction of simple sugar molecules binding to proteins is known as glycation. Showing potential cause of skin and bone damage in a rat model of diabetes, investigators suggested "that long-term fructose consumption negatively affects the aging process." Another study using human proteins showed that the glycation caused by fructose appears to be equivalent to glucose and so does not seem to be a better answer for diabetes for this reason alone, save for the smaller quantities required to achieve equivalent sweetness in some foods. It also found evidence for glycation of human lens proteins caused by fructose.
The people most at risk of increased triglycerides and fat storage from eating fructose are those who are consuming more calories than they need. Consumption of high-fructose corn syrup is also a huge risk factor for anyone, healthy or overweight.
If you eat fruits, and you should, be sure your daily calorie intake is in check and that you are exercising regularly. Then, try to choose fruits lower in sugar, such as apples, berries, melons, and so on, that also offer good nutrient and antioxidant benefits.