Fructose has recently been the focus of much interest as a possible contributor to the current epidemic of metabolic diseases. What is fructose, and why is it implicated in metabolic disease?
Most of us believe that fructose is the healthy part of sugar and we go on consuming hundreds of litres of fruit-juice, honey and other sugars. But what is fructose really? The information provided by the Department of Physiology, and Service of Endocrinology, Diabetes and Metabolism, Faculty of Biology and Medicine, University of Lausanne, 7 rue du Bugnon, CH-1005 Lausanne Switzerland :
Fructose is a hexose with the same chemical formula, C6H12O6, as glucose. These two sweet-tasting molecules differ structurally, however, as fructose has a keto-group on the second carbon while glucose presents an aldehyde group on the first carbon. Free fructose, together with free glucose, is present in small amounts in fruits and honey. The main part of today’s dietary fructose intake comes from sucrose, a disaccharide composed of one molecule of glucose linked to a molecule of fructose through an alpha 1-4 glycoside bond.
The link with metabolic disease is partly circumstantial. Fructose consumption has been low throughout most of human history, but started to increase after the crusades, when Europeans became acquainted with sucrose produced from sugar cane in Asia. It was at first a luxury product, but consumption rapidly increased in the 16th and 17th centuries when sugar became more widely available as a consequence of colonial trading. Its consumption was boosted, first by the introduction of new beverages – tea, coffee, and cocoa in the 17th to 18th centuries; and second with the production of chocolate bars, ice-creams, and sodas at the beginning of the 20th century. Total sugar consumption thus increased from less than 5 kg/person/year in the 1800s to about 40 kg at the turn of the 19th century, and about 70 kg/person/year in 2006. In short, a rapid and continuous increase in consumption has been observed from 1750 until the present day.
In the 1960s, a novel food technology allowed the large-scale, industrial conversion of glucose into fructose. As a result, the US corn industry started preparing what is now known as high fructose corn syrup (HFCS), that is, a concentrated solution of corn-derived glucose and fructose mixed in various relative proportions. Mainly because of its low cost, HFCS consumption replaced approximately one-third of the total sugar consumption in the USA between 1970 and 2000, paralleling to some extent the increasing prevalence of obesity during this period. Consequently, HFCS has been a particular focus of possible blame for the obesity epidemic. However, HFCS consumption has remained very low in other parts of the world where obesity has also increased, and the most commonly used form of HFCS contains about 55% fructose, 42% glucose, and 3% other sugars, and hence is associated with similar total fructose and glucose intakes as with sugar. Furthermore, sucrose is hydrolyzed in the gut and absorbed into the blood as free glucose and fructose, so one would expect HFCS and sucrose to have the same metabolic consequences. In short, there is currently no evidence to support the hypothesis that HFCS makes a significant contribution to metabolic disease independently of the rise in total fructose consumption.
So why the focus on fructose in particular?
Several reasons. First of all, fructose is not essential for any physiological function that we know of. This is in contrast to glucose, which is used by all cells in the body to generate energy and constitutes the nearly exclusive energy fuel for the brain. As a consequence of this largely exclusive reliance on glucose for brain metabolism, intricate hormonal and neural mechanisms have evolved to maintain a constant level of glucose in the blood.
We do not need to eat sugar to maintain blood glucose levels, however. Until relatively recently, our dietary source of glucose was derived from complex carbohydrates, principally from grains. Grains contain starch, which is a polymer of several thousands of glucose molecules linked together by alpha 1-4 glycosidic bonds, with occasional branching points due to alpha 1-6 glycosidic bonds. Cooked starch can be readily digested by amylase produced by the salivary glands and pancreas, resulting in the formation of maltodextrins (small chains of four to nine glucose molecules), maltose, isomaltose, or triomaltose in the gut lumen (see Figure 1). These compounds are subsequently digested into glucose by brush border enzymes of the duodenum and jejunum. Ingestion of starchy products therefore provides a plentiful supply of glucose, which, upon absorption into the circulation, can be used as an energy source by most cells, or be stored as glycogen in the liver and in muscle.
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Tappy L: Q&A: ‘Toxic’ effects of sugar: should we be afraid of fructose? BMC Biology 2012,10:42