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This medical research arises from the pandemic problem of fructose in our processed food, which is the major cause of Non-alcoholic fatty liver disease (NAFLD), which accompanies the terrible scale of modern obesity. This hepatitis-related obesity carries high risks of dementia, cirrhosis, and cancer. The effects are similar to those of alcoholism, but awareness of risks is even lower. This study identifies fructose as doing its damage by causing changes to the barrier function of the intestine, which is a new understanding of how the liver-disease starts. The study proposes the idea that a genetic intervention might, at some time in the future, prevent these changes to some degree, in people very seriously affected. It points to genetic interventions in mice made ill by high fructose-induced diets. The authors of the study note that it would, of course, be better not to ingest the fructose. We have also embedded a video about fructose from the U of California.

[Candobetter Ed: NAMES FOR FRUCTOSE: Fructose is a component of sugar (sucrose). The following ingredients all contain fructose: Brown sugar, corn sweetener, corn syrup, dextrose, fructose, glucose, high-fructose corn syrup, honey, lactose, malt syrup, maltose, molasses, raw sugar and sucrose.]

A team of international researchers including Monash University academics has discovered that, contrary to previous belief, fructose causes liver toxicity by changing the barrier function of the intestine.

The new study, published today (August 25th) in Nature Metabolism, shows that fructose affects the liver only after it causes intestinal barrier disruption, therefore treatments that prevent barrier disruption could protect the liver from fructose-induced diseases including non-alcoholic fatty liver disease (NAFLD), fibrosis and cancer.

Fructose is a simple sugar which can be found in high quantities in soft drinks, sauces and fast foods. With the advent of modern biochemistry and metabolic analysis, in recent times scientists have discovered that fructose is up to three times more potent than glucose in increasing liver fat.

Excessive fructose consumption has been linked to the recent surge in Nonalcoholic fatty liver disease (NAFLD) - one of the most common metabolic disorders - and its associated co-morbidities, which include liver failure, cirrhosis, and cancer.

Australian metabolic disease expert, Professor Mark Febbraio from Monash’s Institute of Pharmaceutical Sciences, was part of the international team of researchers led by Professor Michael Karin from The University of California San Diego, School of Medicine.

Professor Febbraio says:

“The findings from this study make it clear that fructose does its damage in the intestine and if intestinal barrier deterioration is prevented, the fructose does little harm to the liver.”

The intestine is an organ that makes up part of the gastrointestinal system (more commonly known as the gut). In recent years it’s become evident that excessive fructose metabolism in the gut reduces the production of proteins that maintain the gut barrier, which can lead to a chronic inflammation condition called endotoxemia, as documented in animal studies and paediatric NAFLD patients.

The international team of researchers found that by adding a cell signalling protein called ‘tumor necrosis factor’ (TNF) to hepatocytes stimulates the metabolism of fructose and increases the production of the enzymes that convert the molecule ‘acetyl CoA’ to fatty acids.

“A large increase in the expression of these enzymes was also detected in livers of fructose-fed mice,” says Professor Febbraio. “Conversely, genetic modification that reduced TNF production was found to protect mice from fructose-provoked NAFLD, which is a very exciting step forward for the treatment of diseases which can evolve from this all too common liver disorder.”

Although education and increased awareness are the best solutions to the problem of fructose-induce liver disease, for those individuals who progress to the severe form of NAFLD, known as non-alcoholic steatohepatitis (NASH), the findings described in this study offer some hope of a future therapy based on gut barrier restoration.

This study clearly demonstrates that maintaining gut barrier integrity is a therapeutic target to treat liver disease associated with high fructose consumption.

The researchers will now focus on screening drug candidates that target key proteins in the maintenance of gut barrier integrity.

The full study can be found at: https://www.nature.com/articles/s42255-020-0261-2