How fructose in the diet contributes to obesity

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Consumption of fructose appears to alter cells in the digestive tract in a way that allows it to assimilate more nutrients, according to a preclinical study by investigators from Weill Cornell Medicine and New York-Presbyterian. These changes could help explain the well-known link between rising fructose consumption worldwide and rising rates of obesity and certain types of cancer. White sugar (granulated sugar) is known as sucrose and consists of two simple sugar molecules: glucose and fructose. Therefore, any food that contains sugar will also contain fructose.

The research, published in the journal Nature on August 18, focused on the effect of a fructose-rich diet on the hairy, thin, hair-like structures that cover the inside of the small intestine. The villi expand the surface of the intestine and help the body absorb nutrients, including dietary fats, from food as it passes through the digestive tract. The study found that mice that were fed diets that included fructose had villi 25% to 40% longer than those who were deprived of it. In addition, increased hair length has been associated with increased nutrient absorption, weight gain, and fat accumulation.

“Fructose is structurally different from other sugars, such as glucose, and is metabolized differently,” said lead author Dr. Marcus DaSilva Goncalves, endocrinologist and assistant professor of medicine at the Division of Endocrinology, Diabetes and Metabolism at Presbyterian Medical Center. / Weill Cornell of New York. “Our research has found that the major metabolite of fructose promotes the elongation of villi and supports the growth of intestinal tumors.”

Investigators did not intend to study the villi, but previous research by the team, published in 2019, found that fructose in the diet could increase tumor size in models of colorectal cancer mice and that blocking fructose metabolism could prevent this. Arguing that fructose could also promote hyperplasia or accelerated growth of the small intestine, the researchers examined tissues from fructose-treated mice or a control diet under a microscope.

After noticing that the villi were longer, the team wanted to determine if those villas worked differently. So, they placed the mice in three groups: a normal, low-fat diet, a high-fat diet, and a high-fat, fructose-rich diet. Mice in the third group developed longer villi and, at the same time, became more obese than mice that received a high-fat, fructose-free diet.

The researchers looked more closely at changes in metabolism and found that a specific metabolite of fructose, called fructose-1-phosphate, accumulates at high levels. This metabolite interacted with a glucose metabolizing enzyme, called pyruvate kinase, to alter cellular metabolism and facilitate survival and elongation. When pyruvate kinase or the enzyme that produces fructose-1-phosphate was removed, fructose had no effect on the length of the villi. Previous animal studies have suggested that this fructose metabolite also helps in tumor growth.

The observation that mice with a high fructose diet increased the length of their villi, which was made by Samuel Taylor, a student of Dr. Goncalves’ laboratory, was a unique surprise. Then Taylor and Goncalves set out to find out more.

According to Taylor, observations in mice make sense from an evolutionary perspective. “In mammals, especially mammals that hibernate in temperate climates, fructose is very available in the fall months, when the fruit is ripe,” he said. “Consumption of fructose can help these animals absorb and turn more nutrients into fats, which they need to get in the winter.”

Dr. Goncalves added that people have not evolved to eat what they eat now. “Fructose is almost ubiquitous in modern diets, whether it comes from fructose-rich corn syrup, table sugar or natural foods like fruit,” he said. “Fructose itself is not harmful, but excessive consumption is a problem. Our bodies are not designed to consume as much as we are used to today.”

Future research will aim to confirm that the results in mice translate into humans. “There are already drugs in clinical trials for other purposes that target the enzyme responsible for fructose-1-phosphate,” said Goncalves, who is also a member of the Sandra and Edward Meyer Cancer Center. “We hope to find a way to reuse them to reduce villi, reduce fat absorption, and possibly slow tumor growth.”

Find out the benefits of a fructose-tempered diet and especially what foods to avoid or reduce in your personal diet with the free Dahna app, created by cardiologists and nutritionists, which you can download from the AppStore or Google Play.

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