Eating fructose seems to alter the cells of the digestive tract in a way that makes it absorb more nutrients, according to a preclinical study by Weill Cornell Medicine and NewYork-Presbyterian researchers. These changes could help explain the well-known link between higher fructose consumption worldwide and increased rates of obesity and certain cancers.
The research
The research, published on August 18th in Nature, focused on the effect of a high-fructose diet on the villi, the thin, hair-like structures that line the inside of the small intestine. The villi expand the surface area of the gut and help the body absorb nutrients – including dietary fat – from food as they pass through the digestive tract. The study found that mice that were fed diets that included fructose had villi that were 25 to 40% longer than those of mice that were not fed fructose. In addition, the length increase of the villi was associated with a higher absorption of nutrients, weight gain, and fat accumulation in these animals.
The findings
“Fructose is structurally different from other sugars like glucose, and it is metabolized in a different way,” according to lead author, Dr. Marcus DaSilva Goncalves, Ralph L. Nachman academic researcher; associate professor of medicine in the Division of Endocrinology, Diabetes and Metabolism; and NewYork-Presbyterian/Weill Cornell Medical Center endocrinologist. “Our research has found that the major fructose metabolite promotes the lengthening of the villi and supports gut tumor growth.”
The researchers didn’t plan to look at the villi. Previous research by the team, published in 2019, found that dietary fructose could increase tumor size in mouse models of colorectal cancer, and that blocking fructose metabolism could prevent that from happening. Based on the reasoning that fructose might also promote hyperplasia – or accelerated growth – of the small intestine, the researchers examined tissue from mice treated with fructose or a control diet under the microscope.
The observation that mice on a high fructose diet had increased villi length was made by first author Samuel Taylor, a tri-institutional MD-Ph.D program fellow in Dr. Goncalves’ laboratory, and was a complete surprise. And once he made the discovery, he and Dr. Goncalves set out to learn more.
Further research
After observing that the villi were longer, the team wanted to determine if those villi functioned differently. So they divided the mice into three groups: a normal low-fat diet, a high-fat diet, and a high-fat diet with added fructose.
Not only did the mice in the third group develop longer villi, but they also became more obese than the mice that were fed the high-fat, fructose-free diet.
The researchers took a closer look at changes in metabolism and found that a specific fructose metabolite, called fructose-1-phosphate, was building up at high levels. This metabolite interacted with a glucose-metabolizing enzyme called pyruvate kinase, to alter cell metabolism and promote the survival and elongation of villi. When pyruvate kinase or the enzyme that produces fructose-1-phosphate was removed, fructose had no effect on the length of the villi. Previous studies on animals have suggested that this fructose metabolite also promotes tumor growth.
According to Taylor, the observations in mice make sense from an evolutionary perspective. “In mammals, especially mammals that hibernate in temperate climates, fructose is highly available in the fall months when the fruit is ripe,” Taylor observed. “Eating a lot of fructose can help these animals absorb and convert more of the nutrients into fat, which they need to get through the winter.”
Dr. Goncalves added that humans didn’t evolve to eat what they eat now. “Fructose is almost ubiquitous in modern diets, whether it comes from high-fructose corn syrup, table sugar, or natural foods like fruit,” Dr. Goncalves said. “Fructose is not harmful per se. It is an issue of excessive consumption. Our bodies weren’t designed to eat as much of it as we do”.
Future research will try to confirm that the findings in mice can be translated into humans. “Drugs in clinical trials for other purposes that target the enzyme responsible for producing fructose-1-phosphate are already being used,” Dr. Goncalves said. He is also a member of the Sandra and Edward Meyer Cancer Center. “We hope to find a way to reuse these drugs to shrink villi, reduce fat absorption and possibly slow tumor growth.”
Link: https://www.sochob.cl/web1/la-investigacion-descubre-como-la-fructosa-en-la-dieta-contribuye-a-la-obesidad/
Date: August 21, 2021
Source: https://medicalxpress.com
Reference: Taylor SR, Ramsamooj S, Liang RJ, et al. Dietary fructose improves intestinal cell survival and nutrient absorption. Nature. 2021 Aug 18.
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