The study, which was reported in the journal Nature on August 18, looked at the impact of a high-fructose meal on villi, which are thin, hair-like cells that cover the lining of the tiny intestines. Villi assist the body in better absorbing, particularly nutritional fat, in meals as it travels throughout the gastrointestinal tract by increasing the contact surface of the stomach.
The research discovered that mice fed fructose-rich diets developed villi which were 25% to 40 % bigger than mice given a non-fructose-rich diet. Furthermore, the lengthening of the villus was linked to enhanced nutritional intake, excess weight, and fat storage in the animals.
Obesity-Causing High Fructose In The Diet, Study Shows
Obesity is one of the biggest threats to people irrespective of age group. Diet and lifestyle are the main contributors that lead to obesity. Calorie intake and consumption are the key factors that affect the accumulation of fat in the body and fructose plays a prime role in the food that has more calories in concerning food.
As per preclinical research led by Weill Cornell Medicine and New York-Presbyterian, consuming sugar seems to modify cells in the digestive system, allowing it to draw in even more vitamins.
Such alterations can underlie the well-known association between increasing sugar intake and growing overweight and rates of cancer across the globe.
The researchers had no intention of studying villi. The club’s earlier work, reported in 2019, demonstrated that eating sugar could enhance tumor size in mice forms of colon cancer and that inhibiting sucrose conversion can avoid this.
The scientists looked at cells from mice fed sucrose or a simple sugar under the lens, thinking that glucose would induce hyperplasia, or faster development, of the small bowel.
“Fructose is structurally different from other sugars like glucose, and it gets metabolized differently,” said senior author Dr. Marcus DaSilva Goncalves, the Ralph L. Nachman Research Scholar, an assistant professor of medicine in the Division of Endocrinology.
Diabetes and Metabolism and an endocrinologist at New York-Presbyterian/Weill Cornell Medical Center. “Our research has found that fructose’s primary metabolite promotes the elongation of villi and supports intestinal tumor growth.”
According to Taylor, the observations in mice make sense from an evolutionary perspective. “In mammals, especially hibernating mammals in temperate climates, you have fructose being very available in the fall months when the fruit is ripe,” he said. “Eating a lot of fructose may help these animals to absorb and convert more nutrients to fat, which they need to get through the winter.”
After noticing that the villi are larger, the researchers sought to see if they are operating properly. As a result, scientists divided mice into 3 parts: reduced, elevated, and large with additional sugar.
The mice and in the third category just only developed larger villi, but they also grew more overweight than the animals on the high-fat, low-fructose diets.
Dr. Goncalves added that humans did not evolve to eat what they eat now. “Fructose is nearly ubiquitous in modern diets, whether it comes from high-fructose corn syrup, table sugar, or from natural foods like fruit,” he said. “Fructose itself is not harmful. It’s a problem of overconsumption. Our bodies were not designed to eat as much of it as we do.”
Future research will aim to confirm that the findings in mice translate to humans. “There are already drugs in clinical trials for other purposes that target the enzyme responsible for producing fructose-1-phosphate,” said Dr. Goncalves,
who is also a member of the Sandra and Edward Meyer Cancer Center. “We’re hoping to find a way to repurpose them to shrink the villi, reduce fat absorption, and possibly slow tumor growth.”