Over the past several decades, the use of dietary sugar sweeteners like fructose and sucrose — which is enriched in soft drinks and processed foods — has increased tremendously. Moreover, high-fructose corn syrup (HFCS) has become the most widely used sweetener in the U.S., comprised of a 40% glucose and 60% fructose blend. It is widely found in many of today’s low-cost food selections, and has been proposed to greatly contribute to several metabolic diseases and obesity.
Senior investigator Yuri Sautin, PhD, a Diabetes Institute affiliated diabetes researcher and Associate Professor of Medicine, recently examined the effects of a high-fructose corn syrup diet in mice who lacked a key enzyme known as ketohexokinase (KHK); which works to metabolize fructose entering the liver and stores it as fat. Over time, this fat can accumulate and lead to non-alcoholic fatty liver disease (NAFLD), insulin resistance in the liver, and type 2 diabetes — Learn more about the UF Type 2 Diabetes research program here.
Most notably, mice who genetically-lacked this key enzyme were able to redirect fructose consumption through alternate pathways and remained lean with normal insulin sensitivity and healthy distribution of fat in their tissues. Fructose was found to only be stored as fat in the liver while in the presence of KHK.
The study (which Sautin co-authored) was featured in an editorial piece in the October edition of the prestigious Nature Magazine. The segment, entitled “F stands for Fructose and Fat” is a compilation of new research evidence arguing the causative effects of excess fructose intake as a primary mechanism in the development of NAFLD and subsequent metabolic diseases including type 2 diabetes.
The editorial suggests that at one point in time, “fructose conversion to fat may have been advantageous,” citing fruit consumption prior to a harsh ensuing winter as an example. “…Storage of the abundant fructose as fat rather than glycogen could have facilitated survival through the months of low food availability.” But food is rarely limited in the western world at any time of year nowadays.
“This study demonstrates that blocking KHK and redirecting fructose metabolism to alternative pathways is an effective way to prevent visceral obesity and insulin resistance induced by high fructose, a widespread component of Western diets,” said Dr. Sautin.
“Future studies investigating the role of fructose and KHK in the etiology of NAFLD appear warranted.”
For more information about this study, please see the complete publication online. Note: you must have access to the PubMed database.