Sucrose, the primary sugar in human diets, is made up of glucose and fructose. While glucose is an essential source of energy for human cells, minimal foods contain this single sugar. Conversely, fructose (also called fruit sugar) is found naturally in fruits.
However, most of the fructose we eat comes from sucrose (table sugar) and high-fructose corn syrup in breakfast cereals, soft drinks, beverages, sweets, pastries, sauces, condiments, and even savoury ready meals.
Once you eat fructose, your small intestine absorbs it and transports it to the liver, where it is quickly processed. Most fructose is converted to glucose, but the remainder forms other compounds, such as fat, if consumed excessively.
The sugar industry and scientists sponsored by them will have you believe otherwise, but the quantities of sugar we consume these days is concerning.
Many studies have linked sugar to obesity, a risk factor for many chronic diseases, including type 2 diabetes, cardiovascular disease, and autoimmune diseases. Some scientists even argue that sugar is the cause of these diseases, but that’s a stretch. The overall diet and not one single component of diet causes chronic disease.
That said, sugar is still a significant contributor to the global metabolic disease epidemic, and a new study in mice details how sugar potentially contributes to obesity. Fructose seems to change cells in the small intestine such that they absorb more nutrients, leading to weight gain and fat accumulation.
The study, “Dietary fructose improves intestine cell survival and nutrient absorption,” was published in Nature.
The small intestine contains thin, hairlike structures called villi that expand the gut’s surface area and help the body absorb nutrients from food as they pass along the digestive tract.
A team of researchers at the Weill Cornell Medical Centre in New York have previously found that in mouse models of colorectal cancer, excess fructose in the diet promotes intestinal tumour growth and causes villi to elongate and absorb more nutrients, including fat. Removing fructose from these mice diets prevented tumour growth and villi elongation.
Based on these findings, the team decided to investigate if these villi functioned differently. To do this, they put mice into three groups and fed each group a different diet: a standard low-fat diet, a high-fat diet, and a high-fat diet with added fructose. Interestingly, the mice in the third group developed the longest villi and were the most obese.
When the researchers investigated the pathways responsible for these metabolic changes, they found a fructose derivative –fructose-1-phosphate– was accumulating at high levels. This compound worked with pyruvate kinase (an enzyme required for glucose breakdown) to alter cell functioning and promote villus survival and elongation. The blocking of pyruvate kinase or the enzyme needed for fructose-1-phosphate production eliminated fructose’s effect on villus length.
While lead author, Samuel Taylor, was surprised by the finding, he provided an evolutionary explanation. “In mammals, especially hibernating mammals in temperate climates, you have fructose being very available in the fall months when the fruit is ripe. 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,” he said in a press release.
However, Marcus DaSilva Goncalves M.D., Ph.D, assistant professor of medicine in the Division of Endocrinology, Diabetes and Metabolism and an endocrinologist at New York-Presbyterian/Weil Cornell Medical Centre believes that current diets are not in line with evolution.
“Fructose is nearly ubiquitous in modern diets, whether it comes from high-fructose corn syrup, table sugar, or from natural foods like fruit. 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,” he said.
Although future research in humans is necessary to corroborate the findings in mice, “there are already drugs in clinical trials for other purposes that target the enzymes responsible for producing fructose-1-phosphate,” Dr Goncalves said. “We’re hoping to find a way to repurpose them to shrink the villi, reduce fat absorption and possibly slow tumour growth,” he added.
“Fructose is structurally different from other sugars like glucose, and it gets metabolized [processed] differently. Our research has found that fructose’s primary metabolite promotes the elongation of villi and supports intestinal tumour growth,” Dr Goncalves said.
