NAFLD is the world’s most common cause of chronic liver disease. It has the potential to develop into more serious illnesses such as cirrhosis, liver cancer, liver failure, and death. These findings suggest a strategy for preventing liver injury in the first place.

Excessive use of fructose, a common sweetener in the American diet, can lead to non-alcoholic fatty liver disease (NAFLD), which is also common in the country.

However, contrary to popular belief, researchers from the University of California San Diego School of Medicine discovered that fructose has a negative impact on the liver only after it reaches the intestines, where it disrupts the epithelial barrier that protects internal organs from bacterial toxins in the gut.

Since the introduction of high fructose corn syrup (HFCS), a cheaper sugar replacement that is widely used in processed and packaged foods, from cereals and baked goods to soft drinks, fructose consumption in the United States has skyrocketed. Increased HFCS consumption has been linked to the nation’s obesity pandemic and a variety of inflammatory illnesses, including diabetes, heart disease, and cancer, in both animals and people. The US Food and Drug Administration, on the other hand, regulates it similarly to other sweeteners like sucrose or honey, and recommends that it be consumed in moderation.

The results of a study, on the other hand, pinpoint HFCS’s involvement and danger in the development of fatty liver disease.

“The ability of fructose, which is plentiful in dried figs and dates, to induce fatty liver was known to the ancient Egyptians, who fed ducks and geese dried fruit to make their version of foie gras,” said the authors.

“With the advent of modern biochemistry and metabolic analysis, it became obvious that fructose is two to three times more potent than glucose in increasing liver fat, a condition that triggers NAFLD. And the increased consumption of soft drinks containing HFCS corresponds with the explosive growth in NAFLD incidence.”

The enzyme fructokinase, which is produced by both the liver and the gut, breaks down fructose in the human digestive tract. Researchers discovered that excessive fructose metabolism in intestinal cells reduces the production of proteins that help to maintain the gut barrier, which is a layer of tightly packed epithelial cells covered in mucus that keeps bacteria and microbial products like endotoxins from leaking out of the intestines and into the bloodstream.

“Thus, by deteriorating the barrier and increasing its permeability, excessive fructose consumption can result in a chronic inflammatory condition called endotoxemia, which has been documented in both experimental animals and pediatric NAFLD patients,” added the study’s first author Jelena Todoric.

The researchers discovered that endotoxins that made their way into the liver caused an increase in the production of inflammatory cytokines and accelerated the conversion of fructose and glucose into fatty acid accumulation.

“It is very clear that fructose does its dirty work in the intestine,” they wrote, “and if intestinal barrier deterioration is prevented, the fructose does little harm to the liver.”

The researchers discovered that feeding mice a lot of fructose and fat causes them to have a lot of health problems.

“That’s a condition that mimics the 95th percentile of relative fructose intake by American adolescents, who get up to 21.5 percent of their daily calories from fructose, often in combination with calorie-dense foods like hamburgers and French fries,” the researchers added.

Surprisingly, when fructose intake was reduced below a particular threshold, no negative effects in mice were identified, implying that only excessive and long-term fructose consumption poses a health concern. Moderate fructose consumption through normal fruit consumption is well tolerated.

“Unfortunately, many processed foods contain HFCS and most people cannot estimate how much fructose they actually consume,” according to the study authors. “Although education and increased awareness are the best solutions to this problem, for those individuals who had progressed to the severe form of NAFLD known as nonalcoholic steatohepatitis, these findings offer some hope of a future therapy based on gut barrier restoration.”

Source: 10.1038/s42255-020-0261-2

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