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New data on fructose-sweetened beverages and hepatic metabolism

According to figures published by the World Health Organitzation (WHO), in the year 2015 some 2.3 bn adults will be overweight and more than 700 million will suffer from obesity, a pathology which is increasingly being seen in children.

In addition, for some time now the high incidence of obesity in developed countries has coincided with an increase in the consumption of beverages sweetened with fructose, a powerful sweetener. A team from the University of Barcelona (UB) has recently published a study in the journal Hepatology which provides clues to the molecular mechanism through which the fructose in beverages may alter lipid energy metabolism and cause fatty liver and metabolic syndrome.

The study was led by Dr Juan Carlos Laguna of the Department of Pharmacology and Therapeutic Chemistry at the Faculty of Pharmacy, who is also the director of the research group “Nuclear receptors regulating energy metabolism as pharmacological targets”, with the participation of Núria Roglans, Laia Vilà, Mireia Farré, Marta Alegret, Rosa Mª Sánchez and Manuel Vázquez-Carrera.

This preclinical study published in Hepatology was carried out with laboratory rats receiving fructose- or glucose-sweetened liquid intake. No solid food was given. “The fructose in fruit has nothing to do with this study,” stresses Professor Laguna. “Fruit is healthy and its consumption is strongly recommended. Our study focuses on liquid fructose intake as an addition to the ordinary diet.”

Fructose is mainly metabolized in the liver, the target organ of the metabolic alterations caused by the consumption of this sugar. In this study, rats receiving fructose-containing beverages presented a pathology similar to metabolic syndrome, which in the short term causes lipid accumulation (hypertriglyceridemia) and fatty liver, and at later stages hypertension, resistance to insulin, diabetes and obesity.

The fructose used to sweeten beverages alters the lipid metabolism in the liver and, according to the authors, represents a calorie overload to which the body’s metabolism is unable to adapt. Specifically, fructose increases fat synthesis in the liver and reduces its degradation through action on a specific nuclear receptor (PPARa), which controls fatty acid ß-oxidation. “The most novel finding,” says Laguna, “is that this molecular mechanism is related to an impairment in the leptin signal. Leptin is a hormone that plays a key role in the body’s energy control; among its peripheral actions, it accelerates fat oxidation in the liver and reduces its synthesis.”

The study shows that rats receiving beverages with fructose have an excess of leptin in blood. Curiously, though, the liver does not show the effects that one would expect in the presence of high levels of this hormone. It seems that the deficit in the degradation of the fatty acids in the liver may be related to the leptin resistance, which affects a transcription factor (Stat-3) involved in the signalling pathway of leptin in the liver and the hypothalamus. Nor were significant weight differences found between the rats drinking liquids with glucose or fructose, “possibly because this was a short-term experiment and there was no time to detect such changes,” notes Professor Laguna.

Poorly balanced diets and the lack of physical exercise are key factors in the increase of obesity and other metabolic diseases in modern societies. In epidemiological studies in humans, the effect of the intake of fructose-sweetened beverages seems to be more intense in women. Professor Laguna’s team intends to continue research on a variety of fronts: the study of the difference in response between sexes; the study of the molecular mechanisms of leptin resistance in the liver in rat models; experimental studies with hepatocyte cell cultures, and, further into the future, pilot studies of a fructose-rich diet in humans to find possible markers of metabolic alterations in blood cells.

Rosa Martínez | alfa
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