12 January - 20 June 2016

Short term calorically controlled consumption of a high fructose, low fat diet

3 July 13

A study published in the American Journal of Clinical Nutrition has assessed chronic ad libitum and short term calorically controlled consumption of a high fructose, low fat diet (24% of calories) using monkeys.   The first study by Kavanagh et al from Wake Forest Baptist Medical Center studied monkeys who were allowed to eat as much as they wanted of a low-fat food with added fructose for seven years, as compared to a control group fed a low-fructose, low-fat diet for the same time period. The scientists found that the animals allowed to eat as much as they wanted of the high-fructose diet gained 50 percent more weight than the control group. They also developed diabetes at three times the rate of the control group and developed hepatic steatosis, or non-alcoholic fatty liver disease.  To investigate whether it was obesity or whether it was fructose that caused the non–alcoholic fatty liver disease, Kavanagh et al. carried out a second short term study.   Ten middle-aged, normal weight monkeys, who had never eaten fructose, were divided into two groups based on comparable body shapes and waist circumference. Over six weeks, one group was fed a calorie-controlled diet consisting of 24 percent fructose, while the control group was fed a calorie-controlled diet with only a negligible amount of fructose, approximately 0.5 percent.  Both diets had the same amount of fat, carbohydrate and protein, however the sources were different.  The high-fructose group's diet was made from flour, butter, pork fat, eggs and fructose (the main ingredient in corn syrup), while the control group's diet was made from healthy complex carbohydrates and soy protein.  Every week the animals were weighed and their waist circumference measured, then the team adjusted the amount of food provided to prevent weight gain. At the end of the study, the researchers measured biomarkers of liver damage through blood samples and examined what type of bacteria was in the intestine through faecal samples and intestinal biopsies.   The scientists found that in the high-fructose group the type of intestinal bacteria hadn't changed; however they were migrating to the liver more rapidly and causing damage there (microbial translocation).  They note that it seemed that high fructose levels were causing the intestines to be less protective than normal, and consequently allowing the bacteria to leak out at a 30% higher rate.  They conclude by stating that “even in the absence of weight gain, fructose causes liver damage that we suggest is secondary to endotoxemia and microbial translocation.”

RSSL's Functional Ingredients Laboratory can determine fructose by HPLC.  For more information please contact Customer Services on Freephone 0800 243482 or email enquiries@rssl.com

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