According to a new study, eating fructose causes cells in the digestive tract to change in a way that allows it to take in more nutrients. These alterations could explain the association between rising fructose consumption and rising obesity and cancer rates around the world.

Obesity is a complicated, multifaceted, and generally preventable condition that affects 13% of the world's population today. Additionally, 39% of the global population is considered overweight. According to the World Health Organization (WHO), obesity rates have nearly tripled since 1975. If current trends continue, researchers estimate that 38% of the world's adult population will be overweight by 2030, with another 20% being obese. 

According to a recently published study out of Weill Medical College of Cornell University, excessive high-fat corn syrup and processed sugar consumption can lead to increased surface area in the small intestine and increased nutrient absorption when fed a high-fat diet, resulting in increased weight gain.

The new research revealed that mice fed fructose-rich diets had villi that were 25 percent to 40 percent longer than mice fed non-fructose-rich diets. Furthermore, the lengthening of the villus was linked to enhanced nutritional absorption, weight gain, and fat storage in the animals.

The researchers divided the mice into three groups: low-fat, high-fat, and high-fat with additional fructose. The mice in the third group not only developed longer villi, but they also became more obese than the animals on the high-fat, low-fructose diet.

The paper's lead author, Samuel Taylor, suggested a practical evolutionary explanation for the fructose-induced absorption, stating, "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."

The new findings provide a possible mechanistic explanation for previous research regarding the effects of fructose which found that colon polyps feed on fructose, resulting in larger tumors. A study from 2019 stated that data reported in the paper "[supported] the hypothesis that the combination of dietary glucose and fructose, even at a moderate dose, can enhance tumorigenesis."

Dr. Marcus Goncalves, a professor of Endocrinology at Weill Medical College, shared his thoughts on the dangers of fructose, saying, "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."

According to Dr. Goncalves, the research group hopes to use the study's findings to find ways to shrink the villi, reduce fat absorption, and possibly slow colorectal tumor growth.

The study was published in Nature, on August 18th, 2021.

Abstract. Fructose consumption is linked to the rising incidence of obesity and cancer, which are two of the leading causes of morbidity and mortality globally. Dietary fructose metabolism begins at the epithelium of the small intestine, where fructose is transported by glucose transporter type 5 (GLUT5; encoded by SLC2A5) and phosphorylated by ketohexokinase to form fructose 1-phosphate, which accumulates to high levels in the cell. Although this pathway has been implicated in obesity and tumour promotion, the exact mechanism that drives these pathologies in the intestine remains unclear. Here we show that dietary fructose improves the survival of intestinal cells and increases intestinal villus length in several mouse models. The increase in villus length expands the surface area of the gut and increases nutrient absorption and adiposity in mice that are fed a high-fat diet. In hypoxic intestinal cells, fructose 1-phosphate inhibits the M2 isoform of pyruvate kinase to promote cell survival. Genetic ablation of ketohexokinase or stimulation of pyruvate kinase prevents villus elongation and abolishes the nutrient absorption and tumour growth that are induced by feeding mice with high-fructose corn syrup. The ability of fructose to promote cell survival through an allosteric metabolite thus provides additional insights into the excess adiposity generated by a Western diet, and a compelling explanation for the promotion of tumour growth by high-fructose corn syrup.

Taylor, S.R., Ramsamooj, S., Liang, R.J. et al. Dietary fructose improves intestinal cell survival and nutrient absorption. Nature (2021). https://doi.org/10.1038/s41586-021-03827-2

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